Powdery Mildew☆

M Linde, Federal Centre for Breeding Research on Cultivated Plants, Ahrensburg, Germany
N Shishkoff, Foreign Disease Weed Science Research Unit, ARS/USDA, Frederick, MD, United States
r 2017 Elsevier Inc. All rights reserved.

Introduction

Powdery mildew of roses, a disease thought to have been first described by Theophrastus in 300 BC, is a problem worldwide, in
greenhouses or outdoors, wherever roses are grown. Nearly 40% of the fungicide sprayed on roses is to control powdery mildew.
The disease can cause distortion and death of leaves and shoots, but even a mild case makes plants unsightly (Fig. 1). Powdery
mildew reduces the quality of cut flowers and makes nursery stock less saleable to consumers. Its ubiquity causes gardeners and
landscapers to think twice about planting roses. In a time when many parks are cutting maintenance budgets and limiting the use
of pesticides in public places and when the use of many pesticides is restricted or not allowed for many breeders and growers of cut
and garden roses in Europe, this disease continues to be one of the major scourges of roses. In this article we will describe the
pathogen causing powdery mildew, its hosts, symptoms of the disease and how it spreads and the means of controlling it.

The Pathogen

Powdery mildews are classified in the Class Leotiomycetes (with primitive cup-fungi), the Order Erysiphales and the Family
Erysiphaceae. The Erysiphaceae include 16 genera and probably about 400 species. Powdery mildews are obligate parasites; they
can't survive without a living host. Unlike most plant pathogen fungi, which grow within plant tissue, powdery mildews live
epiphytically on the outer surface of plants in mats of whitish hyphae. The hyphal strands are anchored to the leaf surface by pegs
that penetrate epidermal cell walls and form feeding structures called haustoria which allow the absorption of nutrients from leaf
tissue. Vegetative hyphae called conidiophores grow away from the leaf surface and produce spores in chains from their tips, giving
the colony its characteristic powdery appearance (Fig. 2). The fungus also produces spherical structures called ascomata that
contain the sexual spores. These are occasionally visible in colonies as reddish-brown dots.
The species causing powdery mildew of rose had long been known as Sphaerotheca pannosa var. rosae; recent changes in
nomenclature result in the pathogen now being called Podosphaera pannosa (Wallr.: Fr.) de Bary. There is some degree of host
specialization among isolates of P. pannosa, so that isolates from rose tend to be less damaging on Prunus, and vice versa. However,
morphologically distinct varieties do not appear to exist in the pathogen, so it is appropriate to divide isolates into pathotypes to
denote differences in pathogenity on rosaceous genera and species.

Infection Process

The pathogen spreads almost exclusively by the distribution of conidia by wind. Powdery mildew conidia deposited on a
hydrophobic plant surface excrete an adhesive matrix within minutes of contact. The conidia germinate with one or two thick-

Fig. 1 Powdery mildew on a highly susceptible cultivar.

☆
Change History: April 2016. N. Shishkoff updated the text and added “Further Reading” section to this article.

Reference Module in Life Sciences doi:10.1016/B978-0-12-809633-8.05026-3 1

2 Powdery Mildew

Fig. 2 Mycelium and a conidiophore of Podosphaera pannosa on the surface of a rose leaf (raster electron microscope).

walled germ tubes 2–6 h after deposition on the leaf surface. After penetration of the host and establishment of the first
haustorium, mycelium continues to spread along the leaf surface and is the starting point for the development of a fungal colony.
Optimal conditions for germination are around 221C and nearly 100% humidity. Temperatures above 301C prevent germi-
nation. Incubated in moist conditions, conidia can withstand long periods of 01C without loss of viability; survival at 0–31C for up
to 3 months has been described. Germination under lower humidity is also possible down to 50%, but with lower frequency. The
direct contact of conidia with large drops of free water in the first 6–8 h after infection reduced the number of germinated conidia
which grew to a sporulating colony, possibly by a water layer between the host surface and the conidia. Leaf wetness seems not to
inhibit the production of germ tubes in the first 6 h.
After extension of the germ tube, a nipple-shaped unlobed appressorium is produced at the apex. The appressorium is firmly
attached to the cuticle of a host cell by a fine slime layer. A very fine hypha called a penetration peg emerges through a pore of the
appressorium and, with a combination of enzymatic degradation and mechanical force, pushes through the cuticle and host cell wall,
entering the lumen of the epidermal cell. The penetration peg enlarges to an elongated structure, the haustorial neck. Further expansion
of the hypha forms the haustorium. These globose, multilobed structures are the feeding organs of the pathogen. They are formed at
regular intervals as hyphae continue to grow along the surface of the leaf. The haustorium looks as if it is surrounded by an invagination
of the host plasmalemma and cell wall, but is in fact surrounded by an extrahaustorial membrane that is distinctly different from the
rest of the host plasmalemma and by an extrahaustorial matrix, which is distinctly different from the host cell wall (lacking cellulose
and pectin) and the fungal cell wall (not containing chitin). The haustorium, extrahaustorial membrane and matrix together are
referred to as the haustorial complex, and function as an isolated compartment because of an impermeable wall region around the
haustorial neck called the neck band. Water, minerals and metabolites from the host leaf are exported to the haustorium, where they are
used for the pathogen’s growth and spore formation. The intense metabolic activity of the haustorium complex is suggested by the
presence in the haustorium of many elongated mitochondria and an enlarged nucleus in a dense ribosome-rich cytoplasm.

Races of the Pathogen

Physiological races of plant pathogenic fungi are classically defined by differences in virulence of individual isolates of the
pathogen species on a differential set of host genotypes. For this, it is essential to use isolates derived from single conidia (and
therefore of a single genotype) and to test these isolates on appropriate host plants under identical conditions.
Single spore isolates of powdery mildew fungi can be derived in various ways: one possibility is to transfer single conidia or
conidiophores from naturally infected leaves to mildew-free leaves (leaves from in vitro plants or leaves from the greenhouse
wiped off with 70% ethanol) from a susceptible genotype. After about 2–3 weeks single conidia from colonies can be transferred
to new leaves. This process should be repeated several times because of possible contamination by conidia from more than one
conidiophore. Another method is to blow a few conidia from naturally infected leaves on to the susceptible leaf material using an
inoculation tower (Fig. 3). After about 5–10 days, leaves with only single mildew colonies are used as the conidia source for a
second inoculation of mildew-free leaves in the tower. The resulting single colonies are assumed to be single-spore isolates.
Separate forms of P. pannosa were reported in the mid 20th century based on disease frequency in peach orchards. In the 1960s
inoculation experiments with a differential set of host genotypes were made, but not using monoconidial isolates. First reports of
races of P. pannosa using the method mentioned above are from 1984. In a collection of nine isolates from different rose genotypes,
five races of P. pannosa were identified by their significant variation in virulence. Different races of P. pannosa were also identified from
isolates collected from a very limited area. Five isolates were taken from naturally infected genotypes from the plantations of the
 Powdery Mildew 3

Fig. 3 Inoculation tower with rose leaves in Petri dishes in front.

Table 1 Differentiation of races of Podosphaera pannosa

Rose genotype Single-spore isolatea

1 2 3 4 5

95/13–39 þ b
þ þ þ þ
Spalier 3 þ þ   þ
93/1–119 c þ   
“Rebell kordana”  þ þ þ þ
“Queen Elizabeth”  þ  þ 
Rosa multiflora þ þ þ  þ
“Elina”  þ  þ þ
“Pariser Charme” þ þ þ  þ
a
Origin of the isolates: 1–4: Federal Centre for Breeding Research on Cultivated Plants, Ahrensburg, Germany; 5: Risoe National Laboratory, Denmark.
b
Resistant rose genotype (genotypes with only single conidiophores were treated as resistant).
c
Susceptible genotypes: mean values from 3–5 replicated experiments 10 days after inoculation with B2 conidia mm2.

Federal Centre for Breeding Research on Cultivated Plants in Ahrensburg (Germany) and one from the Risoe National Laboratory in
Denmark. Within these six monoconidial isolates, five races could be distinguished, including the Danish isolate, using a differential
set of eight rose genotypes (Table 1), suggesting a differentiation of P. pannosa races in a small geographic area on different rose
genotypes. More recently pathotypes of P. pannosa have been characterized by differences in rDNA sequences.

Susceptibility of Rose Cultivars

Each year several new rose cultivars are brought into the market, many of them bred to have a high degree of resistance against
P. pannosa as well as for the horticulturally important characters desired by consumers, like flower color and architecture or the
4 Powdery Mildew

vase-life of cut flowers. However, only a few display a high level of disease resistance. This may be due to the development of new
genetic races of P. pannosa that can overcome this resistance. Several publications have rated differences in susceptibility of various
cultivars. Among these cultivars few possess complete resistance. And the situation is even worse if we look not only at the natural
infection of cultivars in the field, but also take into account the results from artificial inoculation experiments. Reports concerning
a different degree of susceptibility between the different horticultural classes are not consistent in the literature. Whereas some
authors tend to say that climbing roses, ramblers and hybrid teas are more susceptible than wichurianas, others conclude that
floribunda and polyantha cultivars are generally more susceptible than hybrid teas. In a survey of 120 rose varieties commonly
cultivated in Poland, miniature cultivars like “Zwergkönig 78,” “Fresh Pink,” “Eleanor” or “Degenhard” were far less susceptible
than hybrid teas or floribunda and polyantha cultivars.
In the wild species there seems to be no clear distinction in powdery mildew resistance among the taxonomical sections within
the subgenus Eurosa. Whereas some members of the sections Caninae (Rosa agrestis, Rosa glutinosa) and Pimpinellifoliae (Rosa foetida
var. persiana, Rosa omeiensis var. pteracantha) seem to be highly resistant in field observations with natural infections and artificial
inoculation experiments, there are some species in these sections which are highly susceptible (Rosa britzensis, Rosa vosagiaca ¼ Rosa
caesia subsp. glauca in the Caninae and Rosa pimpinellifolia in the Pimpinellifoliae).

Disease Symptoms

The appearance of infected tissue depends on many factors, including when it was infected. Rose leaves are most susceptible in the
3 days following unfurling. When young, rapidly expanding tissue is infected, it may become stunted or distorted (Fig. 4). Fungal
colonies on young tissue expand quickly, mostly starting on the upper-leaf epidermis. Sometimes they coalesce to cover the entire
surface of a leaf, giving it a whitish appearance. Badly infected tissue will frequently shrivel and die. When older, less susceptible
tissue is infected, colony expansion is slower and leaves will appear normal except for discrete circular fungal colonies. As colonies
age they stop producing conidia and become thicker and feltier. Primary (young) mycelium of P. pannosa shows a cell wall
structure similar to that of the conidia (it is colorless and thin-walled); the persistent secondary mycelium is dense and pannose,
forming a greyish felt of sparsely branched, thick-walled hyphae.
Symptoms may vary from cultivar to cultivar. In some cultivars only leaves and young shoots are infected; in others the stems
may also become felted. Buds can become infected, and even opened flowers, especially in some cultivars of miniature roses.
In resistant cultivars infection may be limited to a few cells that quickly die, killing the fungus with them, causing a brown flecking
of tissue, called hypersensitive response (discussed below).
Environmental conditions also affect the appearance and severity of the disease. Optimum conditions are found on warm,
humid days without rain and cool nights with high humidity. Closely planted roses, roses grown in shade or cultivars with dense
foliage are also susceptible because of poorer air circulation, allowing moist air to remain around plant surfaces for longer
amounts of time.

Spread of Disease Outdoors

The life cycle of P. pannosa is shown in Fig. 5. In autumn, P. pannosa infects dormant buds and overwinters in them. When the buds
unfurl in early spring, the fungus is already present on the young leaves and begins to produce asexual spores called conidia, whose
genetic makeup is identical to the parent colony. In dry weather mature conidia are captured by gusts of wind and blown away.
Spores that land on young rose tissue form additional colonies. Depending on temperature, a conidium can germinate, form a

Fig. 4 Rose leaves showing distortion caused by infection by powdery mildew.

 Powdery Mildew 5

colony and produce new conidia in 4–10 days. Thus the disease spreads with amazing speed. The production of asexual spores
continues throughout the summer as long as there is young tissue to infect. Raindrops knock conidia out of the air and off leaves,
reducing inoculum levels, and large droplets of water on leaves inhibit conidial germination, so long periods of rainy weather will
inhibit powdery mildew (although it will promote the spread of most other fungal pathogens).
In late summer, if both mating types of the fungus are present, the sexual state may form. The fruit bodies of the powdery
mildews are spherical or flattened ascocarps (e in Fig. 5). They are initiated by fusion of the sexual organs of the fungi, the
androgamocyst and the ascogonium, which develop on lateral branchlets of the mycelium (d in Fig. 5). The cells fuse to form a
dikaryon, and ascocarp tissue derived from the ascogonial stalk cell covers the developing proascus. Karyogamy and meiosis result
in 4–8 ascospores in one ascus. The formation of ascocarps by P. pannosa does not occur regularly and is rather erratic. In field
observations ascocarps were only found on less than 5% of over 700 rose species and cultivars investigated over several seasons in
the UK and the US. More ascocarps were detected on old bush roses and ramblers than on modern hybrids, suggesting the
presence of host factors influencing their formation. In addition, many powdery mildews require cool temperatures in autumn to
trigger ascocarp formation, and this may also be the case with the rose powdery mildew. Therefore, in roses, overwintering of the
sexual stage seems to be of little importance. However, if it occurs it increases the chances of genetic recombination.
Weather-forecasting models have been developed to identify periods when environmental conditions favor disease develop-
ment, based on measurements of temperature, leaf wetness and relative humidity. It may be possible to use such models to reduce
the number of fungicide treatments while achieving the same level of control.

Spread in the Greenhouse

Epidemics in greenhouses begin with the introduction of infected plant material or by conidia blown in from outdoors.
Greenhouse conditions are ideal for spread of conidia; air circulation is good enough to disseminate spores but not enough to
keep humid air from accumulating around plant surfaces. Conidia can also be spread on the hands and clothing of greenhouse
workers, and possibly by gnats and whiteflies. Once a greenhouse is infested with mildew, the only sure way to clean it is to
remove all roses from it, wait long enough for any conidia to settle from the air and die, and then reintroduce clean material. It can
be difficult to be sure that a plant is “clean,” particularly in the early stages of infection, or in a resistant cultivar with few
symptoms. Even in a clean greenhouse, infection can occur from conidia produced elsewhere entering through air vents. Recently
manipulation of photoperiod length, light intensity and exposure to UV has shown promise in reducing powdery mildew severity
in greenhouses.

Fig. 5 The life cycle of Podosphaera pannosa. In autumn, P. pannosa infects dormant buds and overwinters in them (a). When the buds unfurl
in early spring, the fungus is already present on the young leaves and quickly forms colonies that produce asexual conidia (b). In dry weather the
conidia are captured by gusts of wind (c); spores that land on young rose tissue form additional colonies. In late summer, if both mating types of
the fungus are present, the sexual state will form (d). Although this step has not been reproduced in the laboratory, it is likely that in spring the
sexual spores are released on to young rose tissue (e).
6 Powdery Mildew

Control by the Plant's Own Defense Mechanisms

After the deposition of the conidia on the leaf, the first barrier to overcome is the cuticle of the leaf and the epidermal cell wall.
Differences in resistance against powdery mildew cannot be explained by cuticle thickness, and penetration of the cells is
apparently not prevented by any morphological barrier.
The first active reaction of the rose leaves against powdery mildew seems to be the development of a papilla. Papillae are cell
wall appositions that form between the plasma membrane and the outer epidermal cell wall of the host under the site of an
appressorium and penetration peg. Cytoplasmic aggregates of organelles and vesicles seem to play a major role in the deposition
of the papilla. Callose, phenolics, proteins, lignin and other compounds have been detected in the papilla. In roses, papillae are
found about 1 h after penetration of the epidermal cell wall, often associated with a restricted development of the penetration peg.
The detailed working mechanisms of the papilla have not been clear up to now. However, the penetrating hyphae are sometimes
stopped in incompatible taxa due to papillae preventing successful colonization.
The development of a collar from fibrillar-granular material around and along the haustorial neck is another feature of the host
reaction to the fungal pathogen. The host cell wall modifications consist of an amorphous area with relatively low cellulose
content surrounded by cellulose-rich fibrillar layers. There seems to be a strong correlation between the occurrence of a collar and
the poor development of haustoria, maybe due to preventing a close association between the extrahaustorial membrane and the
neck wall. If powdery mildew mycelium has penetrated the papillae and has not been stopped by a collar, the fungus may still be
restricted by a hypersensitive response (HR). The HR is a type of programmed cell death of a single host cell or a group of host cells
due to the mildew attack. In barley this happens only if a race-specific resistance gene in the host matches a corresponding
avirulence gene in the fungus. The activation of the pathway to the HR requires the presence of a haustorium in the epidermal cells.
Then there is probably a contact between the avirulence gene products of the pathogen, so-called elicitors, and the resistance gene
products, which serve as the sensory apparatus of the plant.
Epidermal cells of roses and barley which died hypersensitively by an incompatible mildew race exhibit a characteristic
fluorescence, due to callose incorporation into the cell wall and accumulation of phenolic compounds in the cell (Fig. 6).
Single cell death occurs rapidly after penetration, when the fungus had only contact with one or two plant cells. In contrast,
multicell HR starts after limited fungal growth with several haustoria; it is visible by eye and is called a necrotic lesion. The
occurrence of single or multicell HRs seems to depend on a particular combination of avirulence and resistance genes in fungus
and host. The damage of the plant cell membrane seems to be an early event in the HR, followed by the accumulation of phenolics
and a halt to cytoplasmic streaming after 15–18 h. The final stage is cellular collapse at 18–26 h after inoculation in barley. Since
the fungus is dependent on living host cells, it is likely that cell death due to the HR can kill powdery mildew.

Control by Chemicals

The asexual conidia are “clones” which are identical to the parent. However, they are produced in such abundance that chance
mutations may occasionally occur, in perhaps 1 in a million spores. Of those mutated spores, perhaps one in a million has an
advantageous mutation, such as a reduced sensitivity to a given fungicide. Of those spores, perhaps one in thousands lands on a
rose leaf and infects. This may seem like poor odds for pesticide resistance to develop, but over the course of a season so many
spores are produced that resistance will almost invariably develop in a few years unless growers alternate between different control

Fig. 6 Conidia with appressoria and the penetration peg on an epidermal rose cell showing a fluorescence of the cell wall indicating a
hypersensitive response.
 Powdery Mildew 7

Fig. 7 Genetic map of the putative resistance gene Rsp-1 and the linked amplified fragment length polymorphism (AFLP) marker.

methods to make sure that a spore that survives one method will be killed by the subsequent one. Therefore it is important to
understand how each type of control measure works.
Many modern fungicides work by interfering with a single site in a metabolic pathway of the pathogen. If one uses a single
fungicide to control powdery mildew, spraying frequently, the vast majority of spores will be killed. However, a single mutation
altering the shape of one enzyme might be enough to endow a conidium with resistance. The mutant pathogen will have no
competition for space on the now pristine rose leaves and will spread rapidly. Alternating between two pesticides in the same class
is not much better than using a single fungicide, because the two fungicides have similar modes of action. Fungicides like
strobilurins (Compass, Heritage and Cygnus) are not only less toxic to nontarget organisms than older fungicides, they have a
different mode of action from older classes of chemicals like triazoles. Because they are also single-mode-of-action fungicides, they
should not be used alone; they should be incorporated into a management scheme. One should alternate single-mode-of-action
fungicides (like strobilurans and triazoles) with those having broader modes of action: copper compounds, sulphur compounds,
bicarbonate salts, horticultural oils, antifungal plant extracts (such as neem extract, milsana and cinnamite), biocontrol agents
(Ampelomyces quisqualis Cesati ex Schlechtendahl (AQ10 Biofungicide), Pseudozyma flocculosa (Traquair, LA Shaw & Jarvis) Boekhout
& Traquair, Trichoderma harzianum Rifai (Topshield)), and activated-resistance compounds. Some of these may be phytotoxic,
others are less effective than traditional fungicides, but many can be used effectively as one part of a management scheme.
Biocontrol agents generally need higher levels of moisture to infect than the powdery mildews they parasitize, but under
greenhouse conditions it may be possible to manipulate the environment to make them effective.

Control by Breeding Resistant Cultivars

One of the most environmentally safe ways to control rose powdery mildew is to cultivate resistant varieties. Identifying molecular
markers closely linked to resistance genes could be a key factor for resistance breeding. Several studies have shown that disease
resistance may be the combination of one or two major factors and a few minor ones. These can be tagged by a quantitative
analysis and quantitative trait loci (QTL) mapping or by the cosegregation of genetic markers and qualitative resistance data.
A putative resistance gene against P. pannosa (Rsp-1) could be mapped using a bulked segregant analysis. A backcross population
of a resistant and a susceptible diploid parent was analyzed for the resistance against a single-spore isolate. The data from the
segregating population were compared with the distribution of genetic markers (amplified fragment length polymorphism or
AFLP) for about 150 different individuals. AFLP-marker linked to Rsp-1 in a distance between 4 and 16 cM could be mapped on
one side of the putative gene (Fig. 7).
8 Powdery Mildew

Integrated Control

In summary, powdery mildew can be reduced by selecting and breeding resistant cultivars (by testing wild species and introducing
their resistance genes by backcrossing with cultivars with traditional methods or using molecular markers: marker-assisted
selection (MAS); phytopathological tests of cultivars under strict conditions), growing them in a site with full sun and good air
circulation to eliminate conditions favoring conidium germination, and providing adequate but not excessive fertilization. Plants
should be inspected regularly to catch the onset of disease and treatment should consist of an alternation of several methods of
chemical control. Single-mode-of-action fungicides should be used with those having broader modes of action in order to reduce
the chance of resistance developing in the pathogen. The usage of weather-forecasting models based on measurements of tem-
perature, leaf wetness and relative humidity to reduce the number of fungicide treatments while achieving the same level of control
is also constructive.

Further Reading

Belanger, R.R., Labbe, C., Jarvis, W.R., 1994. Commercial-scale control of rose powdery mildew with a fungal antagonist. Plant Disease 78, 420–424.
Bender, C.L., Coyier, D.L., 1984. Isolation and identification of races of Sphaerotheca pannosa var. rosae. Phytopathology 74, 100–103.
Braun, U., 1995. The Powdery Mildews (Erysiphales) of Europe. Jena: G. Fischer.
Cobb, G.S., Hanan, J.J., Baker, R., 1978. Environmental factors affecting rose powdery mildew in greenhouses. HortScience 13, 464–466.
Coyier, D.L., 1985. Powdery mildew. In: Strider, D.L. (Ed.), Diseases of Floral Crops, vol. 2. New York, NY: Praeger Scientific, pp. 405–417.
Daughtrey, M.L., Hodge, K.T., Shishkoff, N., 2016. Powdery mildews. In: Ownley, B.L., Trigliano, R.N. (Eds.), Plant Pathology Concepts and Laboratory Exercises, third ed.
New York, NY: CRC Press, pp. 117–141.
Hajlaoui, M.R., Benhamou, N., Bélanger, R.R., 1991. Cytochemical aspects of fungal penetration, haustorium formation and interfacial material in rose leaves infected by
Sphaerotheca pannosa var. rosae. Physiological and Molecular Plant Pathology 39, 341–355.
Horst, R.K., 1983. Compendium of Rose Diseases. St Paul, MN: APS Press.
Kunoh, H., 1995. Host–parasite specificity in powdery mildews. In: Kohmoto, K., Singh, U.S., Singh, R.P. (Eds.), Pathogenesis and Host Specificity in Plant Diseases:
Histopathology, Biochemistry, Genetic and Molecular Bases, vol. 2. Oxford: Elsevier, pp. 239–250.
Leus, L., Dewitte, A., Van Huylenbroeck, J., et al., 2006. Podosphaera pannosa (syn. Sphaerotheca pannosa) on Rosa and Prunus spp.: Characterization of pathotypes by
differential plant reactions and ITS sequences. Journal of Phytopathology 154, 23–28.
Mence, M.J., Hildebrandt, A.C., 1966. Resistance to powdery mildew in rose. Annals of Applied Biology 58, 309–320.
Micali, C.O., Neumann, U., Grunewald, D., Panstruga, R., O'Connell, R., 2011. Biogenesis of a specialized plant–fungal interface during host cell internalization of
Golovinomyces orontii haustoria. Cell Microbiology. 13, 210–226.
Price, T.V., 1970. Epidemiology and control of powdery mildew (Sphaerotheca pannosa) on roses. Annals of Applied Biology 65, 231–248.
Suthaparan, A., Stensvand, A., Solhaug, K.A., et al., 2012. Suppression of powdery mildew (Podosphaera pannosa) in greenhouse roses by brief exposure to supplemental
UV-B radiation. Plant Disease 96, 1653–1660.
Tjosvold, S.A., Koike, S.T., 2001. Evaluation of reduced risk and other biorational fungicides on the control of powdery mildew on greenhouse roses. Acta Horticulturae 547,
59–67.