Towards a Decision Support System for Alternaria (early blight)

Recent articles, for example in the May issue of Potato Review, suggest that management strategies for early blight caused by Alternaria solani will be based increasingly on Decision Support Systems (DSS). So what is the state of play with such systems? In the US they have been developed over a period exceeding 45 years. They are based on the idea that you can stop the disease in its tracks, when the first spots can be seen on the oldest leaves and before these have generated sufficient spores to cause new infections. The development has gone through several stages, each with its own merits:

1 identifying the first points of infection

This requires intensive inspection and you need to be confident that you know what you are looking for. If you identify the disease, after it has had a chance to form fresh spores and new infections, you will be too late.

2 spore trapping

Checking the spore traps is time consuming and there is a risk of a wrong identification, especially if the operator is not familiar with similar Alternaria species.

3 modelling the development of the crop

The first appearance on the oldest leaves is often determined by the age of plants. This can be predicted though simple day degrees or more complex models for plant development. This system appears to have worked well in central states of the US.

4 modelling the progress of infection by the fungus

The most desirable of systems, because it will avoid the need for spraying when conditions are unfavourable. This requires the measurement of the conditions which are favourable to to infection and spread (relative humidity, temperature, rainfall and leaf wetness). Similar systems have been developed for late blight and the two have been integrated successfully in the US and appear to reflect Alternaria risk well.

Alternaria is a relative newcomer to the UK and therefore there has been little opportunity to evaluate systems in this climate. It is therefore not surprising that UAP have announced that they will use spore traps as a basis for recommendations. The presence or absence of spores is a common sense indicator. The reports that Forecast-Xtra, the late blight DSS, will include early blight as well, suggests that we may be moving in the direction of a full pathogen model.

Meanwhile there are a few practical guidelines:

• Closely watch the lower leaves of crops during and towards the end of the rapid growth stage and expansion of the primary stem

• We have little objective information on which varieties are most susceptible but lots of anecdotal information. Markies appears one of the worst varieties followed closely by Estima and Saturna. Other varieties to watch out for are Cultra, Hermes, Lady Rosetta, Maris Piper, Mimi and Russet Burbank.

• Make sure that you have symptoms checked out by a competent lab. Alternaria alternata causes similar symptoms but is less agressive. There are several other foliage diseases, which can complicate the picture especially late in the season, when the foliage is less tidy. Examples are grey mould (Botryotinia fuckeliana), white mould (Sclerotinia sclerotiorum) and Verticillium wilt (Verticillium dahliae)

Dickeya solani, no ordinary blackleg

Last year many of us heard for the first time about the aggressive form of Dickeya, provisionally named Dickeya solani. First seen in the Netherlands and now found in several West European countries, a handful of cases were reported in England last year. It has always been a complicated business to get to grips with the complexity of symptoms (blackleg, stem rot,wilting, tuber wet rots) associated with a complexity of causal organisms. It is even more complicated when scientists change the names of these organisms. Until now we have been familiar with blackleg, caused by Pectobacterium atroseptica (old name Erwinia carotovora supsp. atroseptica) and blackleg-like symtoms, often accompanied by wilting, caused by a group of species known as Dickeya (old name Erwinia chrysanthemum). Until recently outbreaks in the UK have been found to be caused by Dickeya dianthicola and really only found in crops grown from Dutch seed or crops originating from Dutch seed. The new form has been described as more aggressive, more likely to infect at lower levels and more likely to transmit from plant to plant along rows and even across rows.

This season I was shown a crop of Marfona, which showed blackleg-like symptoms, but with a severity that immediately suggested that this was no ordinary blackleg. The stem rots often affected every stem of a plant, completely arresting the development of this plant shortly after tuber initiation. At least 40% to 50% of plants were affected and the field showed large areas of bare land as a result. Losses may well be in excess of these figures, since the performance of the remaining plants, even if they developed no symptoms later, would be badly affected by the uneven crop stand.

The seriousness of this disease is such that growers would do well to insist on UK, Safe Haven sourced seed. The alternative is to have seed tested. However no testing scheme can give complete assurance because a sample is never going to give 100% accuracy. FERA estimate that whith 3 samples of 200 tubers, the confidence of detecting 0.5% vascular infection, is 95%. A 100 tuber sample will only give a broad indication of high, medium and low risk. The bacteria can apparently infect plants through the roots. Transmission from diseased plants also appears to take place through the vascular system (for Pectobacterium atroseptica this is usually through the breakdown of the seed tuber and contamination of tubers through the soil).

Tobacco Necrosis Virus in potatoes

The fact that this disease occurs only rarely is little consolation when it has messed up your crop. The culprit is a virus which is transmitted by a soil borne fungus Olpidium brassicae. Something to do, you might think, with Brassica crops but there is little evidence that the disease is worse after a Brassica crop. In fact our knowledge about this disease and what are the predisposing conditions are quite limited. It has been recorded in the Netherlands since 1924, where the name ABC disease was adopted after the way in which the symptoms were first descibed viz. (A) dark, slightly raised, dark brown patches, (B) dark, almost sunken patches often resembling horseshoes and (C) lighter groups of brown patches with often parallel cracks. Apparently the virus is not transmitted from seed to daughter tubers. Eersteling (Duke of York), Doré and Bintje appear to have been most frequently affected. A couple of cases have been brought to my attention in the UK in recent years, one in Markies and another in Melody.

Clearly anyone who has had the experience of a spoiled crop as a result of this virus will wish to prevent a repeat. So how much do we really understand about the causal agent? Tobacco Necrosis Virus (TNV) can cause bean stipple streak, tulip necrosis and cucumber mosaic and is also found infecting roots of a wide range of species without causing symptoms. Transmission is through the zoospores of Olpidium brassicae, a soil born fungus. It is capable of forming resting spores , which survive for many years and these may account for the unexpected way in which the disease occasionally crops up. In order for disease to occur there has to be a resident population of the fungus which carries the virus.

There are a lot of things we do not know about the disease. For example can symptomless tubers transmit disease? We have no indication of the proportion of fields which have either the fungus with or without the virus. What part do the resting spores play? So any strategy to limit the spread is highly speculative, but after an outbreak it makes sense to do whatever is reasonable to prevent fresh fields from becoming contaminated. Transfer of potentially contaminated soil from fields where crops have been affected should be avoided, applying practical hygiene.

Caught out by blight

This article was first published in Potato Review, May 2009, p24 (http://www.potatoreview.com/ )

In the spring of 2007 blight took many people by surprise and new lessons had to be learnt. On June 14, I was asked to look at several outbreaks, around the Cambridgeshire – Suffolk border, which appeared to have common features. Four outbreaks occurred in the same district in crops grown from a single seed stock. Three of these were a mere 5 weeks from emergence and of particular interest because at that stage the outbreaks could be easily examined. The infections could be readily spotted by the collapsed state of the foliage. Each patch consisted of about 4 to 5 plants in a row. The infection appeared to have initially taken hold around the first or second leaf axil above ground and spread along the stems, thereby, as it were, snapping the stem. Because the canopy had barely closed, spread was along the row but not across rows. I estimated that the infection was at least 2 to 3 weeks old. From the website http://www.blightwatch.co.uk/ it was possible to estimate that the most likely time of first infection had been about a fortnight after emergence, when a Smith period had been registered and that during the week preceding the identification of outbreak there had been a second prolonged period of high risk, enabling the infection to build up to such damaging proportions.

The question in my mind and that of the agronomist who was looking after the crop was whether this could be a seed borne outbreak? If it had been carried on the wind from outside the crop you might have expected some patches to predominate in one part of a field and not another, especially if the source was nearby. The pattern in which blight had developed in several crops from seed of the same origin was very similar. The patches of infected plants appeared at irregular intervals across each of the fields but with no particular bias to one or other part of each field. If the infection had originated from a seed tuber you might have expected to find a heavily infected single stem in each patch which could be traced to an infected seed tuber but there were none. However, it is not always appreciated that seed borne infection can also be transmitted directly through the soil to stems and leaves above ground. The difficulty is that seed tubers may carry latent (without symptoms) infection and the same goes for underground developing sprouts and stems. These may be activated underground to produce infective spores. On balance, but not with absolute certainty, we concluded that this was most likely seed borne transmission.

What about oospores, the thick walled resting spores we have been hearing so much about? These have a longer lifespan but the evidence to date suggests that these become a problem with short rotations of less than 4 years. This is the experience in the starch potato region of the Netherlands. In this country, progressive growers of premium quality potatoes look for longer rotations, often of 6 to 7 years and this was also the case here. This helps with a number of disease problems but also makes infection from blight oospores unlikely.
What I found instructive about this case was the possibility of looking at the diary of risk periods and fungicide sprays. The risk periods are defined by the blightwatch.co.uk website as Smith periods. The diary page shows not only the half (24h) and full (48h) Smith periods but also the humidity (hours above 90%) and minimum temperature data for the other days on the calendar. This is important because whilst it is clear from the diary that many days appear as low risk, it is not the case that blight stops abruptly when the minimum temperature drops a few degrees below the official threshold of 10ºC. So from the data presented on the calendar it is possible to consider days when there may have been some risk. In our case there had been a number of days which were not classed as Smith periods but during which there may have been some expansion of blight from the already established infections. The spray programme had been robust but unable to cope with the early onset of the outbreak. Subsequently we learned that each of the outbreaks we looked at was caused by the aggressive "blue thriteen" strain. We now know that more aggressive strains of blight have spread in the UK making extra vigilance a necessity.

In detailed surveys in the Netherlands over a 6 year period, 36% of outbreaks could be attributed to infected seed. It would be wrong to jump to conclusions that the figure would be similar here. Indeed the Dutch figures show quite a bit of variation with most seed borne outbreaks in the South West and least in the East of the country. It would be useful to know what the figure would be for different parts of the UK. It would also be useful to know the impact of variety resistance and fungicide choice by the seed grower on this figure.
Up to about 1980 blight sprays were not considered necessary until the canopy closed across the rows and this was then modified to along the rows. More recently this was again modified to when plants are as big as “saucers”. Recent experience suggests that this may even be too late.

Climate Change and its potential consequences for stored potatoes

This article is based on a literature review by Paul Gans and Glyn Harper (Sutton Bridge Experimental Unit) commissioned by Potato Council Ltd and was first published in Potato Review, March 2009, p30(www.potatoreview.com)

With improved storage techniques heavy losses due to bacterial and fungal rots are, thankfully, infrequent events. But what if the balance between stored crops and the organisms capable of causing rots were to change? Could similar losses as a result of rotting become commonplace again? To answer that question we might first think about how climate change would impact on potato crops. Generally the effect on average temperatures may seem moderate, at least in the short term. Predictions vary between 0.1ºC and 0.5ºC per decade but you need only think back and compare the hot summer of 2006 with the wet summers of 2007 and 2008 to realise that it is the peaks and troughs which can change the threat of disease dramatically. It is likely that fewer cold springs would lead to earlier planting in many parts of the UK and consequently warmer temperatures at harvest. Changes in weather conditions around harvest time and early loading may change storage techniques and the use of ambient air and refrigeration to cool potatoes in stores.

There is uncertainty about how climate change might impact on diseases of potato crops but the threats come in two forms. On the one hand, there are several tuber rot diseases which appear infrequently. Consequently they have not been studied as well and it is often difficult to tell whether we are looking at opportunists (organisms which exploit breakdown resulting from another cause) or diseases which are kept in check because conditions are not favourable. On the other hand, there are diseases which do not currently occur in the UK. Some of these, like brown rot and ring rot, are already recognised as serious threats and plant health authorities are doing everything they can to prevent their accidental introduction through imports. Others may not be recognised as threats but may become so, because our climate is gradually warming to meet their temperature threshold.

Of the diseases already established in the UK, pink rot and watery wound rot have been described in earlier editions of Potato Review (September and November 2008). Growers in North America are advised to avoid harvesting tubers with temperatures above 18.5ºC and 21ºC in order to avoid pink rot and watery wound rot respectively. These temperatures are not out of range for current normal English summers and the implications are clear.From the limited amount of information about violet root rot and rubbery rot we would expect warmer weather to favour both diseases. Violet root rot is caused by a fungus, Helicobasidium brebissonii (also referred to as H. purpureum). It can cause symptoms in a wide range of crops but is best known from the damage it causes in carrots and sugar beet. Rubbery rot caused by the fungus Geotrichum candidum, appears to be relatively rare but easily recognised. However, it is also found frequently in association with other types of rot as an opportunist. Before ringing alarm bells it would be useful to know how often these two are actually found. Progressive growers and agronomists can help here by following up problems diligently as they occur and seeking good diagnostic advice.

We know a lot about bacterial wet rots as a result of the serious consequences of blackleg caused by Pectobacterium atrosepticum. Many growers in England will also have come across symptoms similar to blackleg but caused by Dickeya dianthicola (previously known as Erwinia chrysanthemi). It prefers warmer temperatures so there is a clear danger that with climate change the risk becomes greater even in Northern England and Scotland. There are other, unrelated, bacteria which are capable of causing rots. Members of the genus Clostridium should be put on the alert list. When in experiments potatoes were infected with a mixture of two pathogens at 16ºC, P. atroseptica predominated in the rotten tissue. At 22ºC Clostridium was dominant. The question is whether the latter has the same capacity to cause rots or is just as aggressive as P. atroseptica, given the right conditions.

Looking across the horizon there are several tuber rot diseases which could cause harm if they became established here. Stem rot is caused by Sclerotium rolfsii and affects both stems and tubers. It was reported in Northern Italy in 2005 and this serves as a reminder that during extreme weather conditions which may only occur infrequently, diseases will travel. Charcoal rot and stem rot (also known as southern blight) are associated with temperatures in the upper twenties and so there is less likelihood of these becoming established in the UK.

With so many organisms apparently capable of causing rots it is important to remember that tubers are basically robust. Minimising damage, correct procedures for curing and avoiding condensation in stores have reduced rots to present levels – these are general principles which will also protect against future threats. Healthy seed and good hygiene will further contribute towards preventing the spread of unwanted diseases. What is needed, though, is a keen eye for anything that seems out of the ordinary and a willingness to track down the cause. This will ensure that any new threats are detected early and in time for appropriate action.

Healthy seed reduces risk of Skin Spot

This article was first published in Potato Review, January 2009, p30 (http://www.potatoreview.com/)

Skin spot is an old disease with which have to live in spite of our knowledge about the disease. Why the concern? A minority of varieties are especially susceptible to the characteristic skin blemish. And because markets are quite specific about filling certain niches with particular varieties the industry is sometimes committed to growing susceptible varieties. Skin spot pustules usually develop during the later part of the storage season. For example, a crop of King Edward stored for packing can turn from being quite presentable in early autumn to showing serious defects around February. As time goes on, skin spot can also seriously influence suitability for crisping.

There is, however, another less visible effect. The fungus which causes skin spot, Polyscytalum pustulans, can kill the growing tips of buds. In serious cases this can result in failure to emerge. In less serious infections it can lead to uneven stem numbers and subsequent variations in tuber size which will be detrimental to the value of the crop. The extent to which this is a problem today is not clear since it is difficult, when stem numbers are low, to track this back to P. pustulans as one of several possible causes. However, it is worth noting the value of recording stem numbers as a barometer of how well a crop is performing. In any case buds are far less likely to be affected once they have started to develop into sprouts. So even for unchitted seed there is a beneficial effect in making sure that at least dormancy is broken and there is some movement in the eyes before planting.

P. pustulans is seed borne so the best way to deal with skin spot is to purchase uninfected seed. Stocks start off in the first and second generation of multiplication as being free from skin spot but over the generations crops will become infected. At first just a few plants will carry the disease but gradually the incidence will increase. You can see the infection in crops as a light brown flecking on the base of the stems. It is for this reason that when I am inspecting seed crops I always look at the condition of the underground part of the plant. Although I would not go so far as to say that you can predict skin spot from these lesions, clear white stems are a good indicator of a healthy crop. In fact, if skin spot has got into a seed crop it is likely that silver scurf is also present, though it does not leave the same tell-tale marks. It is also clear that the incidence of skin spot is quite variable from crop to crop and is probably much lower than it used to be.

There are several factors that might explain why we can expect to see less skin spot today. First of all there are usually fewer generations between the first multiplication for seed and the ware crop. Secondly, seed producers understand the importance of 'dry curing' which means giving wounds a chance to heal while at the same time ensuring low relative humidity (below 90%). Practices vary between different producers. Some use drying tents, letterbox systems or positive ventilation, others rely on the store ventilators to do the job. The third factor is store hygiene cleaning gets rid of the spores which might infect crops and there are some great vacuum cleaners and approved disinfectants available to help manage a clean store.

But how do you know whether you have done a reasonable job? In order to be sure that all the correct measures are in place you need to monitor the crop. The 'eye plug test, which consists of cutting an eye from each of 100 seed tubers and incubating these at high relative humidity so that dormant fungi will develop, is a well established procedure. The technique helped an earlier generation of researchers to understand the basics of skin spot and a number of other diseases. The eye plug test can give variable results depending on the time of year when it is carried out while the spores which cause skin spot are more difficult to recognise than others. It is encouraging, therefore, to hear that Sutton Bridge Experimental Unit, in collaboration with CSL, will be continuing research on molecular diagnostics. A test has already been developed but the work is being extended to establish the robustness of the assay and to obtain more information relating detectable levels of skin spot at harvest with risk of disease during storage. It is to be hoped that such a test will enable agronomists and seed producers to readily monitor whether their efforts to reduce infection have paid off.

There are a number of factors which can determine the incidence of skin spot. Spores can survive in soils for more than seven years but an interval of four or five years is thought to reduce contamination significantly, at least sufficiently so as not to pose a threat to the ware crop. Low storage temperatures (less than 4°C) will encourage the development of skin spot while the sprout suppressant chlorpropham (CIPC) can make the problem worse. This is thought to be because the chemical suppresses wound healing so the advice not to begin CIPC treatment until the crop is fully cured is also relevant to the management of skin spot symptoms. Skin spot can be reduced in storage by applying imazalil (Fungazil 100 SL) at or immediately after harvest. This measure is, however, not as effective as 2-aminobutane and a suitable replacement has yet be found.

• Know the susceptibility of the variety you are growing
• Practice long rotations to minimise soil contamination
• Avoid poorly drained soils
• Use healthy, low generation seed
• Harvest the crop early and ensure that it is well dried
• Ensure good wound healing
• Avoid the use of CIPC soon after harvest
• Avoid reducing the holding temperature below 4°C
• Fungicide to reduce skin spot in store should be applied at or immediately after harvest

Are you recognising Watery Wound Rot?

This article was first published in Potato Review, November 2008, p28 (http://www.potatoreview.com/)

If you look at some text book pictures of watery wound rot, you might think that this is a condition that is easily recognised. The tuber centre often appears grey and wet and the North American name shell rot accurately describes the way in which the rot hollows out the tuber, leaving the outer layer as a shell. However my impression of the disease changed radically when rapid detection kits became available. I found that many difficult to identify rots tested positive for Pythium spp., a group of moulds, one of which, Pythium ultimum, causes Watery Wound rot. I found that often these did not look at all like the text book pictures. One of the reasons we see these complications is because once a tuber starts to rot, other organisms which are lying dormant also become active. One of the principle culprits can be Pectobacterium atroseptica, which causes blackleg. There are several other bacteria which can cause tuber wet rot. The lessons to be learned from this are firstly that we need continuously to carry out tests to corroborate our observations and secondly that watery wound rot may be more widespread than we realise.


In North America, Pink Rot and Watery Wound Rot are often lumped together as “water rots”. This reflects a similarity between the symptoms and also the circumstances under which the diseases occur. Like Pink Rot, Watery Wound Rot is associated with warm weather and damage during harvest. However the critical temperature for Watery Wound Rot is a little higher than that for pink rot. Whereas to prevent Pink Rot, advice in the US is not to harvest until the temperature is below 18.5°C, for Watery Wound Rot this figure is 21°C. Unlike Pink Rot infection appears to be dependent on the presence of wounds. This has a consequence for fungicide protection. Metalaxyl is better at controlling Pink Rot than Watery Wound Rot. The explanation lies in the fact that much initial Pink Rot infection arises from invading zoospores prior to harvest. Most Watery Wound Rot appears to arise from soil contamination of wounds. In this way the disease appears to bypass the metalaxyl barrier. Like for Pink Rot, metalaxyl resistance has been found for Watery Wound Rot. Also like Pink rot there are variety differences offering scope for breeding watery wound rot resistant varieties in the future but there is little choice of variety to avoid the disease today.


Pythium ultimum, the organism which causes Watery Wound Rot, can cause damping-off of seedlings and rotting of roots, stems and fruits of wide range of crops. As far as we know there are no special strains which prefer one crop to another. It forms oospores, sporangia and zoospores and these may be instrumental in long term survival. However it appears to have developed its own special strategy for competing with other soil organisms by germinating whenever there are nutrients available in the soil and then retracting again to a form in which it can survive long term. This strategy may also be the key to manage the disease if only we could understand the positive and negative factors which affect this process. Some soils may simply be unkind to P. ultimum and if we understood why, we could exploit that.

Watery wound rot, on a scale that is reported in North America, is unlikely to be an issue in this country. However the number of cases where watery wound rot has been confirmed raises the suspicion that the organism which causes watery wound rot is around and may be causing more harm than we realise even at below threshold temperatures. Sorting out what has gone wrong, once you are confronted with serious rotting is a complicated business. Fortunately methods for identifying different causal organisms are improving all the time. For some time now there have been kits* which are specific for Pythium spp. and for Phytophthora spp.. This means that they can be used in combination to tell suspected pink rot from suspected watery wound rot, but will not tell the difference between Phytophthora infestans (blight) and Phytophthora erythroseptica (pink rot). The essential measures to manage watery wound rot are similar to those for pink rot. These measures consist generally of damage prevention at harvest and optimal conditions during the early storage period. Additionaly, when things go wrong it is well worth spending some money either on some test kits or on sending a sample to a reputable lab.

• Be suspicious of any wet rot and test for watery wound rot


• Ensure good skin set prior to harvest


• Minimise damage during harvest


• Remember that risk increases with higher temperatures at harvest (21°C is the recommended threshold for harvest in North America)


• Prevent infected tubers from going into store


• Ensure adequate curing to promote wound healing


• Tuber temperatures should be taken to below 10°C as soon as is practicable


• Prevent condensation in store

*Pythium and Phytophthora kits are available from Neogen Europe Ltd, Ayr, Scotland, KA6 5HW. http://www.neogeneurope.com/ and from Forsite Diagnostics Ltd, Sand Hutton, York Y0411LZ. http://www.forsitediagnostics.com/