All posts by ddlang

July: 20 Years in the Life of a Plant Disease Diagnostician

July 1, 2018 marks my 20th anniversary as director of the UW-Madison/Extension Plant Disease Diagnostics Clinic.  It really seems just like yesterday that I started at the clinic.  I remember being so excited about being asked to interview for the position, but terrified that I wouldn’t be hired because my diagnostic background was very limited.  I felt better after I gave my interview seminar and Tom German (a virologist in my department) commented how he didn’t see how I could have given a better talk.  Craig Grau (the department field and forage drop Extension specialist and my boss at the time) was also incredibly supportive, and Jennifer Parke (my previous boss in the department) wrote me (from what I was told) a “perfect” letter of recommendation.

Eventually the stars aligned, I was hired, and I was off to the plant disease diagnostic races on July 1, 1998.  I had only two weeks of overlap with Sr. Mary Francis Heimann (my predecessor in the clinic) and I tried to sop up as much of her knowledge as I could in that short period of time.  After that, it was sink or swim.  In particular, I was forced to learn a lot about ornamental diseases (the bulk of my samples even to this day) very quickly.  Everyone in my department, and also Phil Pellitteri (the UW-Madison/Extension insect diagnostician in the UW-Madison Department of Entomology), was very supportive as I consulted with folks about plants, diseases and insect pests that I was unfamiliar with.  I have learned a lot with everyone I have interacted with over the past 20 years and continue to do so even now.

The PDDC’s physical facilities have evolved over the years as well.  My original clinic space was a small lab and office on the second floor in Russell Labs.  I remember one day when so many samples arrived that I had to leave them in a pile on the floor because there wasn’t enough counter space to organize them.  And then there was the 8 ft. Douglas fir that I had to drag into the hall for several days so I could work in the lab and then haul it back into the lab each night so the custodial staff wouldn’t haul it to the dumpster.  Eventually, I moved to the clinic’s current location in Rm. 183 Russell Labs, about three times the size of my original space.  With the arrival of soybean rust into the US in 2004, I added clean space in the basement of Russell Labs so I could pursue the molecular diagnostics needed to detect the pathogen.  I added a new office just a few years ago and now have about four times my original space.  With renovations, I and my staff have created an efficient and productive work space.

And speaking of staff, I have had the best over the years.  The first addition to the clinic was Lynn Williamson, a returning adult undergraduate, who worked for several years as a student hourly in the PDDC.  As my funding became more stable (with increased clinic revenues and federal funding through the National Plant Diagnostic Network), Ann Joy (who I had worked with previously in the department) joined the clinic as the Assistant Diagnostician, providing general support and initiating our foray into molecular diagnostics.  With Ann’s retirement, Sean Toporek joined the clinic as her successor and expanded the PDDC’s molecular diagnostics over his roughly two year tenure.  With Sean’s decision to pursue graduate school (his MS at the time and now his PhD), Sue Lueloff joined the clinic and our molecular diagnostic program has exploded.  Over the years, an army of dedicated undergraduates have worked (and kept me young) in the lab culminating this year with John Lake (my student hourly) and Stephanie Salgado (a Memorial High School intern hired through the TOPS/AVID program).  Ann Joy continues her presence in the clinic doing data entry and Dixie Lang recently joined the group to provide her magical IT expertise and clinic website ( and social media (@UWPDDC on Facebook and Twitter) support.  Everyone I have worked with over the years including new Plant Pathology faculty and PJ Liesch (Phil Pellitteri’s successor in the Insect Diagnostic Lab), continue to help me learn and do my job.

Clinic activities have expanded over the years.  In addition to diagnosing plant diseases (on average about 1500 samples per year), the clinic provides outreach on plant diseases throughout the state and also nationwide.  I routinely give disease talks (a record 104 in 2017) particularly providing support for home gardeners and professionals in the horticulture arena.  I am particularly grateful to county UW-Extension agents/educators (like Lisa Johnson of Dane County UW-Extension and Diana Alfuth of Pierce County UW-Extension) who have been willing to collaborate with me to provide programming.  I’ve had the pleasure of doing television (on the late Shelley Ryan’s “Wisconsin Gardener”) and radio (on Larry Meiller’s “Garden Talk”) under the moniker “Dr. Death” (a nickname that I acquired at Garden Expo years ago and that makes me smile every time I hear it).  I am also pleased to have been involved in the development of the “University of Wisconsin Garden Facts/Farm Facts/Pest Alert” fact sheet series (  I continue to enjoy instructional activities at the UW-Madison including helping Bryan Jensen with his “IPM Scout School” course and conducting my summer “Plant Disease Diagnostics Practicum” course.

It’s been a great 20 years at the PDDC and I don’t see myself retiring anytime soon.  I still have too much I would like to do.  Diagnostics, my outreach activities and my fact sheet work still call.  In addition, I am currently working on plans for an outdoor plant disease laboratory (in collaboration with James Steiner of the UW-Madison Department of Planning and Landscape Architecture) that I would like to see to completion.  And it has always been my goal, time permitting, to have a more active research program in my department documenting new pathogens (new hosts for Verticillium anyone?).  I am excited as I enter my third decade in the PDDC and look forward to whatever challenges come my way.

As always, if you have questions about plant diseases and their management, or PDDC activities and services, feel free to contact me at (608) 262-2863 or

June: Stormy Weather Ahead – Pathogens on the Wind

Trees in WindJune 1 marks the beginning of Hurricane season in the Atlantic and while full-blown hurricanes do not reach Wisconsin, their effects (and those of other seasonal winds) can have an influence on plant diseases.

Soybean rustA somewhat recent example of an apparent direct effect of a hurricane was the introduction of the Asian soybean rust fungus (Phakopsora pachyrhizi) into the United States in 2004.  Prior to 2004, this fungus had been well-established in South America (after an initial introduction in 2001) and caused substantial losses in soybean production in Brazil.  US soybean producers had been watching this disease closely and were concerned that the pathogen would hopscotch from island to island through the Caribbean and eventually make its way to the US.  The introduction of soybean rust however occurred quite abruptly in 2004.  The speculated method of introduction was by Hurricane Ivan which skirted the coast South American in September and then made its initial landfall in the US in Alabama (as a hurricane) and then made a second, later landfall in Louisiana (as a tropical depression) after reforming following a looped track through Maryland, and then eventually the Florida peninsula.  Soybean rust was first confirmed in Louisiana in November of 2004, roughly two months after Hurricane Ivan.  Losses due to soybean rust in the US have never approached those seen in Brazil, but the disease continues its presence in the southern US to this day.  While soybean rust has never been reported in Wisconsin, spores of the pathogen have been documented in Wisconsin, apparently having been blown into the state by southerly winds.  Fortunately these spores have never led to a soybean rust outbreak.

Black stem rust of wheat:  If you find the idea that spores of the soybean rust fungus can make it all the way from the southern US to Wisconsin amazing, I present for your consideration another amazing example of long distance movement of a pathogen via wind:  black stem rust of wheat.  The fungus that causes this disease (Puccinia graminis) is an alternating rust that requires two very radically different plants, wheat (a grass) and barberry (a broad-leafed shrub), to complete its life cycle (including sexual reproduction).  During this life cycle, spores produces on wheat infect barberry and spores produced on barberry infect wheat.  Attempts (and very successful ones) were made to eradicate barberry from wheat-producing regions of the US starting in 1918.  The thought behind barberry eradication was that eliminating this plant would prevent the black stem rust from completing its life cycle, and thus eliminate the disease.  What folks didn’t count on was a third type of spore that the fungus produces, one that is produced on wheat and reinfects wheat.  This spore type (called a urediniospore) is produced year around in the southern US on wheat, and urediniospores can blow from the south into more northern wheat-producing areas (including Wisconsin) every growing season.  This movement is so well documented that it’s been dubbed the Puccinia Pathway.  Although eliminating barberry did not totally eliminate black stem rust, it did severely limit sexual reproduction of Puccinia graminis.  This is important, because it’s during sexual reproduction that recombination of fungal genes occurs that can lead to new variants of the pathogen that can overcome resistance genes in commercially-grown varieties of wheat.  Genetic resistance is a major means of controlling black stem rust.  Less pathogen sexual reproduction means that resistant wheat varieties tend to be effective longer.

Coneflowers with aster yellows (right) often have deformed, discolored flowers.

Aster yellowsMy final example of a windborne pathogen is an indirect one.  Aster yellows is a disease caused by a bacterium-like organism called a phytoplasma (specifically the aster yellows phytoplasma).  This organism does not survive on its own in the environment, but will survive inside infected living plants.  The host range of the aster yellow phytoplasma is very broad including over 300 plants in roughly 40 plant families.  In addition to residing in infected plants, the aster yellows phytoplasma also can survive in association with certain insects, particularly the aster leafhopper.  This insect does not survive Wisconsin winters, but does overwinter in the southern US.  During the growing season, aster leafhoppers can fly (and/or be blown) to Wisconsin, and some carry with them the phytoplasma.  As the leafhoppers feed in a plant’s phloem (it’s food-conducting tissue), they drop off the phytoplasma, and once in the plant, the phytoplasma induces a wide range of very bizarre symptoms.  These include, but are not limited to, yellow leaves, curled and cupped leaves, leafy-green flowers, tufts of white hairy roots (particularly on carrots), mini-tubers on the branches of infected potato plants and an off flavor to certain edible plants (like carrot).  The year 2012 was a particularly good year for aster yellows.  The season got started early (March), aster leafhoppers arrived early and in larger numbers than usual, and a higher percentage of the leafhoppers carried phytoplasmas than normal.  There were symptoms of aster yellows EVERYWHERE.  I was in plant pathologist’s heaven.  I also distinctly remember talking about this disease in a presentation in Iron County, WI.  The county Extension educator who was hosting me came up after my talk and told me how her little boy, who had always liked carrots, refused to eat them that year because they “tasted funny”.  She said after seeing the photos in my talk, she realized all of her carrots had aster yellows.  Her son had been able to tell.  Amazing!

So, as you enjoy the breezes of late spring and summer, remember that on those breezes are the seeds (or should I say spores) of plant diseases and destruction, some coming from nearby, some coming from afar.  As always, if you have questions about plant diseases and their management, feel free to contact me at (608) 262-2863 or

May: Rattling the Cage for Tobacco Rattle Virus

It’s been a long winter and now temperatures have warmed to the point that spring emphemerals in my backyard are beginning to emerge and bloom.  As their leaves begin to appear, I am on the lookout for symptoms of tobacco rattle caused by Tobacco rattle virus (TRV).

Tobacco rattle virus-infected plants often have leaves with yellow line patterns.
Tobacco rattle virus-infected plants often have leaves with yellow line patterns.

I know I have TRV in my garden and I am reasonably certain that I introduced the virus via a bluebell that a fried gave me many years ago.  The plant showed interesting line patterns on the leaves and a bit of leaf distortion.  If I had been a “good” gardener, I would have thrown the plant away as it had obvious symptoms of a viral disease.  Instead, I was a “good” plant pathologist and plopped the plant into one of my beds and let it do its thing.  Over the years I have seen symptoms of TRV in numerous plants in my backyard flowerbeds.  I have volunteer Canada goldenrod plants that have lightning bolt (think Harry Potter’s forehead scar), yellow line patterns on their leaves every year.  About 10 years ago, I noticed a similar line pattern on leaves on my bleeding heart, odd blotchy color and crinkly of leaves on my bloodroot, and dimpling and distorted leaves on my twinleaf.  I had my visual diagnosis of TRV confirmed by diagnosticians at the Wisconsin Department of Agriculture, Trade and Consumer Protection, who had just started testing for the virus in nursery/greenhouse stock.  My bleeding heart in particular was quite positive for the virus.

The diagnosis and symptoms of TRV fascinated me as a plant pathologist.  However, they horrified me as a gardener because virus-infected plants often decline over time and typically stop blooming as the virus redirects plant energy and nutrients from producing more plant tissue and setting new flower buds to producing more viral particles.  Interestingly though, after that one year of dramatic symptoms 10 years ago, my plants (other than the volunteer goldenrod) have been conspicuously lacking in any symptoms of TRV.  Several years ago, I began testing for TRV in my own clinic and last year I noticed that the stock of positive control material for my test was getting low and I needed TRV-infected tissue to generate more.  My bleeding heart was huge, lush, blooming profusely and totally asymptomatic, but I thought, “What the heck,” let’s test the plant again for TRV.  Lo and behold the test lit up like the proverbial Christmas tree as positive for TRV.  So did the symptomatic goldenrod from my yard.  I had my positive control material.

All of the blathering above about TRV is well and good, but what are the take home messages?

  • Beware of plants showing viral symptoms.  No matter what the virus, these plants can be bad news because they can serve as a source of a virus that eventually end up in other plants.  Interestingly, TRV is transmitted by stubby root nematodes, microscopic worm-like organisms that feed on roots of infected plants, pick up the virus, and then transmit the virus once they feed on the roots of healthy plants.  TRV can also be transmitted mechanically via contaminated tools (e.g., shovels, knives, etc.) used to divide plants.  Nematode-transmitted viruses are somewhat unusual, but mechanically-transmitted viruses are very common.  Another common way that certain viruses (but not TRV) can be moved about is by insects (aphids and thrips are notorious movers of plant viruses).  Some viruses can even be transmitted by touch!
  • Even healthy-looking plants can be infected with TRV.  As my bleeding heart demonstrates, plants that look healthy and bloom profusely can be have a viral problem.  TRV has been a real issue in the perennial plant industry as the virus has a wide host range (including but not limited to the plants I have already mentioned as well as peony, astilbe, coral bells and relatives, and columbine) and often the plants show no symptoms.  The onus is on plant propagators to supply healthy virus-free plants, but often they do not.  So consumers buy TRV-infected, asymptomatic perennials, and happily plant them in their gardens only to have the virus rear its ugly head in other plants as it spreads.  Asymptomatic plants can particularly be a problem if you plant them near a commercial potato field.  Potato is a host for TRV.  The virus does not cause foliar symptoms, but leads to necrotic (i.e., dead) flecks and arcs in potato tubers.  If these tubers are sliced and fried, you end up with potato chips with black spots.  Thus commercial potato producers (FYI, Wisconsin is the third largest potato producer in the US) are very worried about this virus.
  • Proper sanitation is critical for managing this (and other viruses).  Watch for any symptomatic plants and immediately remove and destroy them (by burning, burying or hot composting).  Unfortunately, you may still have asymptomatic plants and the only way to check them for TRV is to have them professionally tested.  This is not an inexpensive test (my clinic currently charges $35 for TRV-testing).  Also, be careful to decontaminate anything (e.g., tools, working surfaces) that may have come in contact with infected plants.  Soapy solutions work best.  I typically recommend a solution that is 10% shampoo (make sure the label says the shampoo contains sodium lauryl sulfate) and 1% Alconox® (a laboratory detergent) in water.

All of this said, you may decide you think TRV-infected plants look cool (I do!) want to leave them in place.  TRV-infected plants are actually quite beautiful.  But be aware that I DO NOT recommend this if you live near a commercial potato field.  And even in urban areas, your neighbors may not be happy with you if the virus spreads to their plants.  Luckily I have neighbors who are tolerant of my plant pathological eccentricities.  You may not be so lucky!  As always, if you have questions about plant diseases and their management, feel free to contact me at (608) 262-2863 or

P.S.:  Happy Belated Robigalia (April 25), the Roman festival of the god of rust!

Pink Eye of Potato

What is pink eye?  Pink eye is a disorder of potato tubers that can cause costly storage losses for potato growers and can reduce tuber quality to the point where tubers will be rejected by potato processors.  Pink eye not only directly affects tubers, but also makes tubers more susceptible to diseases such as Pythium leak, bacterial soft rot (see University of Wisconsin Garden Facts XHT1224), pink rot, and Fusarium dry rot.  These diseases cause additional storage losses and reduction in quality.

Pink eye is characterized by a pink discoloration of the skin of potato tubers.
Pink eye is characterized by a pink discoloration of the skin of potato tubers.

What does pink eye look like?  Pink eye is characterized by a short-lived external pink color that is often, but not always, found around the potato eyes of freshly harvested tubers.  Eyes at the bud ends of tubers (i.e., those farthest from where tubers are attached to stems) more commonly show pink eye symptoms.  Pink eye can eventually develop into corky patch/bull hide, which involves a thickening of areas of tuber skin extending approximately 1/10 of an inch into the tuber flesh.  Corky patch/bull hide can make tubers unmarketable for either fresh market or processing use.

External pink eye symptoms are often accompanied by brown patches in the tuber flesh immediately underneath the skin.  Browning due to pink eye can resemble browning due to other disorders such as internal brown spot or heat necrosis, but these latter disorders tend to occur deeper in the tuber (i.e., inside the vascular ring), rather than just underneath the skin.

Pink eye can also be confused with late blight.  If there is any question whether the problem might be late blight rather than pink eye, contact your county Extension agent for information on submitting a sample to a diagnostic lab for proper testing.

Where does pink eye come from?  Pink eye is a physiological disorder (i.e., an abnormality in plant growth), rather than a true disease that involves a disease-causing microorganism.  Pink eye arises during periods of excessive soil moisture and warm temperatures, especially during the later stages of tuber development.  Pink eye symptoms typically appear within 7 to 10 days after excessive rain.  Excessive soil moisture coupled with high soil temperature causes a lack of oxygen around potato tubers, leading to damage of cells in the tuber skin.  This cell damage

contributes to pink eye development.  Environmental conditions that lead to pink eye also promote tuber infections by the pathogens that cause Pythium leak, bacterial soft rot, pink rot, and Fusarium dry rot (all diseases associated with pink eye in storage).

How do I salvage potato tubers affected by pink eye?  Once pink eye symptoms develop, they are permanent.  If symptoms are minor, tubers may still be usable.  However, when pink eye symptoms are severe, symptomatic tubers will be rejected and discarded.

How do I avoid problems with pink eye in the future?  Growers have no control over the extreme precipitation and high temperatures that promote pink eye development.  However, growers can practice management strategies that minimize water-saturated soils and reduce warm soil temperatures, thus reducing the severity of pink eye.

To minimize water-saturated soils, deep till areas where pink eye has been a problem, areas where water tends to collect for extended periods, and areas where soils may be compacted (e.g., field entrances or head lands).  Deep tillage will break up subsoils in these areas that impede proper drainage during wet weather.  Proper drainage will limit periods when tubers will be oxygen deprived and thus more prone to pink eye development.  Also, avoid any activities that will cause soil compaction such as operation of heavy and large farm tractors and field equipment when soils are wet.  Minimizing water-saturated soils will not only reduce the likelihood of pink eye development but will also help limit development of other tuber diseases.

To promote cooler soil temperatures, be sure to manage diseases (e.g., potato early dying) that reduce canopy coverage.  Loss of canopy allows soils to warm faster on sunny days, thus leading to higher temperatures that are more favorable for pink eye development.

Finally, be sure to scout for pink eye symptoms prior to and during harvest.  Knowing the severity of pink eye in a field can help growers make informed decisions about the appropriate duration for tuber storage and the best end use for symptomatic tubers.

For more information on pink eye:  Contact your county Extension agent.

April: April Showers Bring…Plant Diseases (Yay!)

It appears that spring is slowly arriving, and with the spring typically comes regular, often frequent rain showers.  The upside to this moisture is that it helps thaw the ground and stimulate plants to grow.  The downside however can be that this moisture provides a favorable environment for plant diseases to develop.

Lower stem collapse of Zinnia seedlings due to damping-off.
Lower stem collapse of Zinnia seedlings due to damping-off.

Damping-Off:  If you like to plant early when soils are colder and moisture is high, you may run into problems with damping-off.  Damping-off pathogens (e.g., Pythium, Rhizoctonia, Fusarium) are found, at least at some level, in many soils and when combined with wet conditions and young, tender seedlings, death and destruction can be the result.  Watch for plants that never emerge (the seed rot or pre-emergence phases of damping-off) or those that do and then fall over onto the soil surface with collapsed lower stems (the post-emergence phase of the disease).  You can often avoid damping-off by planting later when soils are warmer and there is slightly drier weather.  The warmer soil stimulates plants to grow rapidly out of early stages of growth when they are most susceptible to infection.  Using a good seed fungicide treatment (often commercial seeds are pretreated prior to packaging) can also help prevent the disease.  Just be sure to handle any fungicide-treated seed according to the directions on the package to minimize any direct exposure to the fungicide.

Brown discoloration of roots typical of root rots.
Brown discoloration of roots typical of root rots.

Root Rots:  Root rots are caused by many of the same organisms that cause damping-off including Phytophthora, Pythium, Rhizoctonia and Fusarium.  Root rots differ from damping-off however in that affect older herbaceous and woody plants.  The pathogens destroy root tissue, thus reducing water uptake, and that can eventually translate into dieback, general plant decline and, in extreme cases, death.  Root rot organisms tend to perform better in wet soils, and Pythium and Phytophthora actually reproduce more efficiently under cooler, wetter conditions.  So, making sure soils are well drained can be critical for root rot prevention.  Adding organic matter to heavier, clay soils to improve drainage prior to establishing a landscape can have a big impact long term on reducing root rot problems.  Also, making sure to mulch properly can help moderate soil moisture to a level that makes root rots less likely.  I typically recommend using approximately one to two inches of a high quality mulch (e.g., shredded oak bark mulch or red cedar mulch) on heavier, clay soils and roughly three inches of mulch (perhaps up to four inches) on lighter, sandier soils.  The mulch should be applied out to at least the dripline of trees and shrubs (i.e., the edge of where the branches extend) and kept away (approximately four to six inches) from tree trunks and crowns of shrubs.

Symptoms of tar spot on silver maple leaves.
Symptoms of tar spot on silver maple leaves.

Leaf Spots and Blights:  Spring rains can also have a huge effect on the severity of many types of leaf spots and blights like anthracnose, tar spot and apple scab.  If extended rainy periods arrive when leaves are first emerging, then numerous infections can occur early and that can translate into severe disease and possibly even defoliation later in the summer.  Luckily trees seem to tolerate at least some defoliation, and long term effects due to leaf diseases are often minimal.  However, defoliation year after year can stress plants to the point where they become susceptible to more serious diseases (e.g., Armillaria root disease) and insect pests (e.g., two-lined chestnut borer).  While we have no control over Mother Nature and the rain she brings in the spring, using other disease management strategies can help lessen the effects of wet spring weather.  Careful cleanup and destruction (by burning, burning or hot composting) of plant debris in the fall can significantly reduce leaf pathogen carryover.  Proper pruning of trees to promote better air penetration, allowing for more rapid drying of foliage can also help reduce problems with leaf diseases.  For certain diseases like apple scab, growing a resistant apple or crabapple variety may be your best option.  And finally, in certain situations, use of preventative fungicide treatments may be warranted to keep leaf diseases in check.

So, as you dream of those warm spring rain, dream of them in moderation.  As with most things in life, balance is the key.  Hope for enough rain to get your plants to grow, but not enough to lead to disease problems.  As always, if you have questions about plant diseases and their management, feel free to contact me at (608) 262-2863 or


Audio Test

March: The Irish – Good Luck in Life, Bad Luck in Plants

As March arrives, being in part Irish by ancestry, my thoughts tend towards St. Patrick’s Day and as a plant pathologist, I imagine what havoc plant disease might cause for the holiday.


ShamrocksA major symbol of St. Patrick’s Day is the shamrock.  While several plants can be called shamrocks, the most common plant to be so-named is white clover (Tifolium repens).  This plant was once a common component of lawns (in combination with grasses such as Kentucky bluegrass) and served the important function of enriching soil with nitrogen.  Interestingly, it’s not the clover plant itself that is instrumental in this nitrogen enrichment process.  Actually, the credit goes to the bacterium Rhizobium which colonizes the roots of clover (along with the roots of other plants in the pea family) and causes formation of nodules (swellings) on the roots.  Inside the pinkish, elongate nodules, Rhizobium takes nitrogen gas (which is very common in the air) and converts it to a form of nitrogen that is more easily used not only by the bacterium, but by the clover plant it colonizes.  In exchange for this ready supply of nitrogen, the clover plants provide Rhizobium with sugars (produced through photosynthesis) that it needs to grow and reproduce.

Root-knot nematodes cause swollen, distorted roots that can interfere with movement of water and nutrients within a plant.
Root-knot nematodes cause swollen, distorted roots that can interfere with movement of water and nutrients within a plant.

This interesting symbiosis between clover and Rhizobium, can be disrupted by the plant pathogenic nematode Meloidogyne, more commonly known as the root-knot nematode.  Nematodes are small (typically microscopic) worm-like organisms.  Many nematodes are beneficial, but root-knot nematode infects the roots of a variety of plants (including clover) causing damage.  Root-knot nematode females tunnel into roots and set up feeding sites.  In the process of feeding, they secrete saliva that stimulates root cells to grow larger than normal, grow faster than normal, and divide like crazy.  This uncontrolled growth leads to a tumor-like swelling on the infected root (called a gall or knot).  Formation of the galls can interfere with root function (i.e., movement of water and nutrients to leaves and stems above ground) and can also interfere with proper nodulation by Rhizobium.  Thus plants with root-knot nematode often look stunted and discolored due to nutrient deficiencies caused by the presence of the pathogen.  You’re not going to find a lot of four-leafed clover leaves on plants with root-knot.



The food that comes to my mind as a symbol of St. Patrick’s Day is corned beef and cabbage.  While I can’t say too much plant pathological about beef, cabbage is another matter.  The primary disease that I can think of that would prevent you from enjoying your cooked cabbage is black rot.  I have seen an amazing increase in the incidence of this bacterial disease over the past five years or so.  The disease not only affects cabbage, but virtually all types of brassicas, the group of plants that includes cabbage, broccoli, cauliflower, kale, rutabaga and turnip, as well as weed plants such as shepherd’s purse and wild mustard.  Often the causal bacterium (Xanthomonas campestris pv. campestris) comes into a garden on contaminated (but asymptomatic) seed or transplants.

Black rot causes V-shaped yellow and brown/ dead areas in affected leaves. (Photo courtesy of Amanda Gevens)
Black rot causes V-shaped yellow and brown/ dead areas in affected leaves. (Photo courtesy of Amanda Gevens)

Eventually wedge-shaped yellow, then dead areas develop on leaves or other plant parts leading to deterioration of the plant.  Black rot can be followed by soft rot (another bacterial disease), leading to even more extensive damage.  It’s not a happy day when cabbage with black rot and soft rot arrives in my clinic.  The stench is overpowering!  Good debris clean up, decontamination of gardening tools, proper weed control, proper vegetable rotation, and hot-water seed treatments can all help in managing this disease.


And no discussion of the Irish would be complete without a mention of late blight, the cause of the Irish potato famine.  This devastating disease wiped out the Irish potato crop for several years in the 1840’s and 1850’s.  For a variety political and social reasons, potato was the primary food of the Irish during this period.  Loss of the crop due to late blight led to the starvation of over 1 million Irish and the emigration of over 1 million more Irish, many of them to the US.  I am sitting, writing this article in Madison, WI due to this disease.

Late Blight on Potato Tubers, photo courtesy of Prof. Amanda Gevens
Late Blight on Potato Tubers. (Photo courtesy of Amanda Gevens)

Even today, late blight can have a huge negative impact on both commercial and home garden potato (and tomato) production.  Without proper treatment the disease can wipe out entire potato and tomato patches/fields in a matter of a few days.  It is critical therefore to identify any occurrences of the disease in Wisconsin as early in the growing season as possible and also identify which variant(s) (and there are many) of the pathogen is(are) causing problems.  For that reason, my clinic provides free diagnoses for late blight for anyone growing potatoes and tomatoes in Wisconsin.  All you need to do to get the free diagnosis is send in a potato or tomato sample and invoke the words “late blight” and the diagnosis is free.  Even if you don’t think your potato or tomato problem is late blight, send in a sample, mention “late blight” and I’ll provide a diagnosis and management recommendations for free.  You can send samples to:

Plant Disease Diagnostics Clinic
Department of Plant Pathology
University of Wisconsin-Madison
1630 Linden Drive
Madison, WI  53706-1598

As always, if you have questions, feel free to contact me at (608) 262-2863 or

With that, go forth, wear green, drink green beer, think about the contributions that the Irish have made to US culture and of course, don’t forget about the all-important plant diseases.  Happy St. Patrick’s Day!!

Shamrock and Claddagh


Improving Cranberry Pollination

Successful cranberry production relies on cranberry flowers being adequately pollinated.  This fact sheet discusses several strategies that can be used to optimize pollination.

Proper pollination is important for successful cranberry production. (Photo courtesy of Johnston's Cranberry Marsh & Muskoka Lakes Winery, Ontario, Canada).
Proper pollination is important for successful cranberry production. (Photo courtesy of Johnston’s Cranberry Marsh & Muskoka Lakes Winery, Ontario, Canada).

Increase and diversify plants attractive to pollinators.  Having both native pollinators and honeybees on your marsh serves as an “insurance policy” to promote good fruit set.  Providing diverse sources of nectar and pollen (e.g., through the use of a pollinator garden), will encourage native pollinators to establish themselves long-term near your marsh and improve the health of honeybee colonies.  When planning a pollinator garden, select a site that is sunny and 1/3 to one mile away from your marsh.  Some common native plants to consider for a pollinator garden are listed in the figure below, with their approximate bloom times.

Promote nesting habitats for wild bees.  Wild bees need places to build their nests.  Approximately 70% of native bees nest underground and need areas of bare, sandy or loamy soil to build their nests.  The remaining 30% build nests by tunneling into stumps or twigs, or by constructing nests in cavities (e.g., in mounds of tall grasses, in debris piles, or in deserted rodent nests).  Native pollinators typically travel from 1/8 to one mile from their nests to feed, so suitable nesting areas need to be within this distance of a marsh for the bees to contribute to cranberry pollination.

Several programs can assist with the costs of creating pollinator habitats.  These include the USDA Environmental Quality Incentives Program, the USDA Farm Service Agency, the Wisconsin DNR Land Owner Incentive Program and the Bayer Crop Science Feed a Bee Initiative.


LEFT: Approximate bloom times for plants that are recommended to be grown near cranberry marshes as a supplemental nectar and pollen source for cranberry pollinators. RIGHT: Approximate flight periods for major groups of bees (including native species) found in cranberry marshes. The pink columns in both graphs represent the approximate time of cranberry bloom.
LEFT: Approximate bloom times for plants that are recommended to be grown near cranberry marshes as a supplemental nectar and pollen source for cranberry pollinators. RIGHT: Approximate flight periods for major groups of bees (including native species) found in cranberry marshes. The pink columns in both graphs represent the approximate time of cranberry bloom.

Reduce pesticide exposureYou can optimize bee health by creating a pollinator protection plan that promotes:

  • Practicing integrated pest management (IPM). IPM, which involves monitoring for pests and using a variety of appropriate management strategies, is used by most Wisconsin cranberry growers.
  • Spraying when bees are least active. Most bees forage from early morning until shortly before sunset. Therefore, the best time to apply a pesticide, especially during bloom (if allowed by the pesticide label), is in the late evening or at night.
  • Limiting pesticide drift. Whether plants are blooming or not, using a boom sprayer allows for direct application of pesticides onto cranberry plants.  Other methods that can reduce pesticide drift include calibrating your boom to optimize spray pressure and volume, selecting drift-reducing nozzles, avoiding pesticides with small particles that easily drift, and spraying when winds are under 10 mph and when relative humidity is above 50%.
  • Using insecticides and fungicides that have a reduced risk for bees. See the table below for insecticides and fungicides that are least toxic for bees.
(IRAC or FRAC code)
Active Ingredient(s)
Trade Names

(IRAC code)*

diamide (28) chlorantraniliprole Altacor
diacylhydrazine (18) methoxyfenozide




biological Bacillus thuringiensis Biobit, Dipel

(FRAC code)*

strobilurin (11) azoxystrobin Abound, Evito
chitin synthase inhibitor (19) polyoxin D zinc salt Oso
biological Reynoutria sachalinensis Regalia

*  Note that rotating Insecticide Resistance Action Committee (IRAC) classes and Fungicide Resistance Action Committee (FRAC) codes (modes of action) will help delay development of pesticide resistance.

Strengthen your working relationship with beekeepers.  Optimal cranberry pollination requires cooperation between grower and beekeeper.  In some cases, outlining expectations in a signed, written contract can be the best way to prevent misunderstandings.  Topics to consider and discuss with your beekeeper can include, but are not limited to:

  • Hive inspections. Inspecting a random sample of 10% of hives when they are brought onto a march can help ensure that hives are of high quality and contain healthy bees.  Ideally, a third party should conduct the inspections in the presence of both beekeeper and grower.
  • When bees are introduced onto a cranberry marsh and the duration of their stay are important factors in optimizing cranberry pollination, as well as for maintaining honeybee health.  Bees should be brought onto a marsh at around 15% bloom.
  • Hive placement. Within the limits of your bed layout and equipment needs, it is best to place hives in the center of a marsh or near marsh edges with wild habitat, but away from water reservoirs, as bees from hive near water seem to be less likely to visit cranberry plants.
  • Exposures to sprays. Be explicit about when, how and what may be sprayed during bloom.

For more information on improving cranberry pollination:  Watch for UW Extension bulletin A4155, “Practices to improve pollination and protect pollinators in Wisconsin cranberry” (available soon at, or University of Wisconsin Garden Facts XHT1213 “Pollinators” (available at, or contact your county Extension agent.

Blueberry Maggot

Blueberry maggot was first detected in Wisconsin in the summer of 2016 in Adams and Sauk Counties.  This pest feeds inside blueberry fruit and caused damage in commercial blueberry production in the eastern and southern United States, as well as in eastern Canada.  This insect is expected to eventually have a significant impact on blueberry production in Wisconsin.

Blueberry maggot adult with characteristic wing patterns (left) and larva (right). (Photos courtesy of Rufus Isaacs, Michigan State University)
Blueberry maggot adult with characteristic wing patterns (left) and larva (right). (Photos courtesy of Rufus Isaacs, Michigan State University)

Appearance:  The adult blueberry maggot is a fly that is approximately 3/16 inch long and resembles a small housefly, but with dark bands on its wings.  Larvae (or maggots) are legless and can grow up to 5/16 inch in length.  Each larva has a single hook-like tooth at its mouth end.  Blueberry maggots are very similar in appearance to the closely related apple maggot, with adults of both being virtually identical in size and appearance (including wing patterns).  However, apple maggot does not feed on blueberries.

Host Range:  Blueberry (Vaccinium corymbosum) is the only commercially-grown fruit crop affected by blueberry maggot.  Wild hosts include plant species in the genera Vaccinium and Gaylussacia including wild blueberries, lingonberry, dangleberry, deerberry and huckleberry.

Symptoms and Effects:  A single larva feeds inside each fruit causing the berry to become soft as it develops.  Damage may go unnoticed until after harvest, when maggots crawl out of fruit and become visible among fresh fruit or in processed blueberry products (e.g., jams, preserves, pie fillings).

Life Cycle:  Adult blueberry maggots begin to fly in June or July, and continue to fly through August.  Females feed and mate for at least one week before they move to blueberry plants to begin laying eggs.  Females lay a single egg under the skin of a nearly ripe blueberry fruit and can lay up to 100 eggs during their approximately one month-long life span.  Eggs hatch within one week and damage from larvae generally first appears in mid-July, continuing until blueberries have been harvested.  Each maggot feeds in a single blueberry during its two- to three-week development.  After completing their development, larvae drop to the ground and overwinter as pupae in the upper few inches of soil.  A distinctive characteristic of the blueberry maggot is that, although most pupae develop to form adults by the following spring (completing one generation of the insect in a year), some pupae remain underground and do not mature for two or three years.

Monitoring:  Monitor for blueberry maggot adults several weeks before blueberries begin to ripen (usually in early June) using yellow sticky cards impregnated with a feeding attractant (ammonium acetate or ammonium carbonate).  You can buy cards that are pretreated with the attractant, or buy the cards and attractant separately and apply the attractant yourself.  Fold the sticky cards in a V-shape with the yellow side facing down and put up two traps for every five acres.  Because blueberry maggot is currently not widespread in Wisconsin, you can check cards weekly until you find the first adult.  After this initial find, check cards every few days.  Once you find an average of greater than one adult per trap for several days in a row, begin chemical treatments (see below).  Note that the feeding attractant is not specific for blueberry maggot, so you may find other types of flies on the cards – use a hand-lens or magnifying glass to positively identify any blueberry maggot adults.  Remember that blueberry maggot and apple maggot look very similar, but that apple maggot does not feed on blueberries, so flies trapped in blueberry fields/patches are most likely to be blueberry maggot.

Once you have detected adults, you can also test fruit for the presence of larvae.  Collect 100 berries from throughout your planting.  Then break the skins of the berries and mix the berries with a salt-water solution (1 part salt to 4 parts water).  Larvae will float to the surface.  The number of larvae you find represents the percentage of fruit infested.

Control:  Cultural control methods can be useful in preventing blueberry maggot infestations.  Remove weeds to eliminate habitat for blueberry maggot.  Remove wild blueberry and huckleberry plants as these can serve as alternate hosts for the insect.  Harvest fruits thoroughly and heat (to at least 120°F) or freeze any damaged or unusable fruits to kill blueberry maggot larvae.  This is particularly important if you compost fruit, because blueberry maggot pupae can readily survive in compost and serve as a source of an infestation in future years.  Clean soil thoroughly from equipment or beehives that might be moved between blueberry patches.  Blueberry maggot pupae can easily be moved in soil.

A blueberry maggot trap. (Photos courtesy of Rufus Isaacs, Michigan State University)
A blueberry maggot trap. (Photos courtesy of Rufus Isaacs, Michigan State University)

As noted above, start chemical control once you find an average of greater than one adult blueberry maggot per trap for several days in a row.  Alternatively, if you have had a serious problem in the past, you may want to start sprays one week after you trap your first blueberry maggot fly.  Continue sprays every seven to 10 days through harvest.  Some reduced risk active ingredients, such as novaluron, spinetoram, and spinosad are most effective when used as soon as flies are found in traps.  In addition, consider choosing a product that also provides control of spotted wing drosophila, another serious blueberry pest (see University of Wisconsin Garden Facts XHT1237 for details).  Spinosyn, spinetoram, diamide, carbamate, pyrethroid, and organophosphate-containing insecticides are effective against both insects.  Be sure to rotate use of at least two active ingredients with different modes of action to help delay development of insecticide resistance (see for details), and be sure consider the effects of sprays on non-target (e.g., beneficial insects).  Finally, because you will be spraying ripe berries, pay particular attention to the pre-harvest interval when choosing insecticides.  Check the most recent Midwest Fruit Pest Management Guide (see for complete product recommendations.

For more information on or help diagnosing blueberry maggot:  Contact your county Extension agent.

February: The Facts Ma’am, Just the (UW Garden) Facts

The winter months are the prime period at the PDDC when staff are able to concentrate on outreach activities that do not involve diagnosing diseases on plant specimens.  One of the major outreach efforts of the PDDC has been and continues to be the University of Wisconsin (UW) Garden Facts fact sheet series.

The UW Garden Facts were originally conceived and developed by the University of Wisconsin-Extension Horticulture Team.  These one-page fact sheets were designed to be user friendly for home gardeners.  They are short, concise and easy to read, with an emphasis on answers to questions that homeowners often ask about horticultural issues.  Due to their popularity, the UW Garden Facts series was eventually expanded to include UW Farm Facts (covering more agriculture-oriented topics) and UW Pest Alerts (covering new and emerging disease/pest issues in both the agricultural and horticultural arenas).

The UW Garden Facts/Farm Facts/Pest Alerts series currently has over 250 titles, all of which are available in several formats for download free-of-charge from the “Fact Sheets” section of the UW-Madison/Extension Plant Disease Diagnostics Clinic website.  A web friendly version of the fact sheets (for reading online) is also available on the website.  If you are a horticulture or agriculture professional and would like to distribute the fact sheets as part of your business (which is encouraged), there is space to customize each fact sheet with personal or business information (e.g., a company logo).

A two CD compilation of University of Wisconsin Facts is also available.  The compilation contains the full set of the fact sheets and costs $30 for the general public and $20 for Master Gardener volunteers, plus shipping and handling (approximately $3.00 per CD).  To order a compilation, contact:

Brian Hudelson
Plant Disease Diagnostics Clinic
Department of Plant Pathology
University of Wisconsin-Madison
1630 Linden Drive
Madison, WI  53706-1598
Telephone:  (608) 262-2863

Complimentary copies of UW Garden Facts/Farm Facts/Pest Alerts are also available in the display outside the PDDC (Rm. 183 Russell Labs at the address listed above), and complementary horticulture-related disease titles will also be available February 9-11, 2018 at the PDDC booth (booth 833-834) at Garden Expo 2018.  To keep up to date on new and revised fact sheets, be sure to follow the UW-PDDC on Facebook and Twitter @UWPDDC, or contact the PDDC at the phone number or email address listed above.

Happy reading!!