Diseases of Poinsettia … · a wealth of foliar problems (Botrytis blight, powdery mildew, scab, Alternaria leaf spot, Xanthomonas leaf spot, andanthracnose) as well as many commonroot

Diseases of Poinsettia

Margery L. Daughtrey and A. R. Chase

Contents1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 Fungal and Fungus-Like Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

2.1 Alternaria Leaf Spot [Alternaria euphorbiicola E. Simmons and Engelhard,Alternaria euphorbiae (Barth) Aragaki and Uchida (comb. nov.)] . . . . . . . . . . . . . . . . . . 3

2.2 Amphobotrys Blight [Amphobotrys ricini (Buchw.) Hennebert (syn. Botryotiniaricini (Godfrey) Whetzel)] . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

2.3 Anthracnose [Colletotrichum truncatum (Schwein.) Andrus and W. D. Moore (syn.C. capsici (Sydow) E. J. Butler and Bisby)] . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

2.4 Botrytis Blight or Gray Mold [Botrytis cinerea (syn. Botryotinia fuckeliana(de Bary) Whetz)] . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

2.5 Choanephora Wet Rot [Choanephora cucurbitarum (Berk. and Rav.) Thaxter] . . . 102.6 Corynespora Leaf and Bract Spot [C. cassiicola (Berk. and M. A. Curtis)

C. T. Wei (syn. Helminthosporium cassiicola Berk. and M. A. Curtis)] . . . . . . . . . . . . 112.7 Fusarium Stem Rot [Fusarium solani (Mart.) Sacco] . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 122.8 Powdery Mildews: Leveillula clavata Nour, L. taurica (Lev.) G. Arnaud,

Pseudoidium poinsettiae (U. Braun, Minnis, and Yañez-Morales), Phyllactiniapoinsettiae, and Ovulariopsis erysiphoides . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

2.9 Pythium Root Rot (Pythium spp.) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 172.10 Phytophthora Crown and Root Rot (Phytophthora drechsleri, P. nicotianae,

P. cryptogea) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 222.11 Rhizoctonia Cutting Rot, Crown Rot, and Root Rot [Rhizoctonia solani Kuhn

(syn. Thanatephorus cucumeris (A. B. Frank) Donk)] . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 232.12 Rhizopus Blight [R. stolonifer (Ehrenb.:Fr.) Vuill. (syn. Rhizopus nigricans

Ehrenb.)] . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 262.13 Scab (Spot Anthracnose) (Sphaceloma poinsettiae Jenk. and Ruehle) . . . . . . . . . . . . . . 28

M.L. Daughtrey (*)Section of Plant Pathology and Plant-Microbe Biology, Cornell University, Long IslandHorticultural Research & Extension Center, Riverhead, NY, USAe-mail: [email protected]

A.R. ChaseChase Agricultural Consulting LLC, Cottonwood, AZ, USAe-mail: [email protected]

# Springer International Publishing AG 2016R.J. McGovern, W.H. Elmer (eds.), Handbook of Florist's Crops Diseases, Handbook ofPlant Disease Management, DOI 10.1007/978-3-319-32374-9_39-1

1

mailto:[email protected]

mailto:[email protected]

2.14 Thielaviopsis Black Root Rot: Thielaviopsis basicola (Berk. and Broome)Ferraris (syn. Chalara elegans) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

3 Bacterial Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 353.1 Bacterial Canker [Curtobacterium flaccumfaciens pv. poinsettiae (Starr and Pirone)

Collins and Jones (Previously Corynebacterium flaccumfacienssubsp. poinsettiae)] . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

3.2 Greasy Canker [Pseudomonas viridiflava (Burkholder) Dowson] . . . . . . . . . . . . . . . . . . . . 363.3 Soft Rot and Stem Rot [Dickeya chrysanthemi (syn. Pectobacterium chrysanthemi)

and Pectobacterium carotovorum (syn. Erwinia carotovora (Jones)) Holland.] . . . . . 373.4 Xanthomonas Leaf Spot [X. axonopodis pv. poinsettiicola (Patel et al. 1951) Vauterin,

Hoste, Kersters, and Swings 1995 (syn. X. campestris pv. poinsettiicola)] . . . . . . . . . . . 383.5 Poinsettia Branch-Inducing Phytoplasma (Candidatus Phytoplasma sp.) . . . . . . . . . . . . 40

4 Viruses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 424.1 Poinsettia Mosaic (Poinsettia mosaic virus PnMV) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 424.2 Poinsettia Latent Virus (PnLV) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

AbstractPoinsettia, Euphorbia pulcherrimaWilld. ex. Klotsch, is a major flowering pottedplant for winter holidays. Because it is vegetatively propagated and is so widelygrown, poinsettia diseases are relatively well known and well studied. Being awoody plant, poinsettias are not prone to tospoviruses, but they are susceptible toa wealth of foliar problems (Botrytis blight, powdery mildew, scab, Alternarialeaf spot, Xanthomonas leaf spot, and anthracnose) as well as many common rootand stem diseases (Pythium and Phytophthora root rots, Thielaviopsis root rot) aswell as occasional Fusarium or Rhizoctonia stem problems. Poinsettia mosaicvirus (PMV) has been associated with minor problems, and a phytoplasmalinfection has contributed free branching for more attractive plants. Poinsettiadiseases may be managed through clean stock production coupled with integratedpest management strategies in greenhouses where the crops are propagated andfinished for sale.

KeywordsPoinsettia • Euphorbia pulcherrima • IPM • Botrytis • Powdery mildew • Scab •Xanthomonas • Pythium • Poinsettia mosaic • Branch-inducing phytoplasma

1 Introduction

Poinsettia, Euphorbia pulcherrima Willd. ex. Klotsch, is a woody plant used as anornamental, especially as a potted plant for the winter holidays. The poinsettia isnative to an area near Taxco, Mexico, where the Aztecs valued it for its red bractcolor and made use of it as a dye and for medicines (Ecke et al. 2004). Poinsettiaswere brought to the United States in 1825 by Joel Roberts Poinsett, the first USambassador to Mexico. The poinsettias sold from the 1920s to 1960s were largelyselections or sports from a single seedling called ‘oak leaf’ grown in New Jersey in

2 M.L. Daughtrey and A.R. Chase

the 1920s, many of them developed by Paul Ecke Sr. in Encinitas, California (Eckeet al. 2004). The plant was developed as an ornamental crop in the United States andEurope in the latter half of the twentieth century, through commercial, university,and federal breeding programs. Their success led to a diversity of bract colors andforms and attractive dark green foliage and branching habit (Ecke et al. 2004). Todaythe poinsettia is the leading potted flowering plant for indoor use, with a wholesalevalue of $141 million in 2014 (USDA 2015). Poinsettias are also used as landscapeornamentals in subtropical areas, including the southern United States. Poinsettiasfor holiday potted plants are produced from cuttings under protective glass or plasticstructures in temperate climates during the summer and fall for late fall sales.

Poinsettias are one of the most important flower crops, thus their diseases havereceived more attention than many. For some of the less common diseases, ourknowledge extends only to identification, while for others research has beenconducted on poinsettias or other hosts to unravel the secrets of their epidemiologyand management (Benson et al. 2001; Strider and Jones 1985). Throughout thischapter, the numeric groupings assigned by the Fungicide Resistance Action Com-mittee (FRAC) will be used to designate mode of action for fungicide activeingredients.

2 Fungal and Fungus-Like Diseases

2.1 Alternaria Leaf Spot [Alternaria euphorbiicola E. Simmonsand Engelhard, Alternaria euphorbiae (Barth) Aragakiand Uchida (comb. nov.)]

2.1.1 Geographic Occurrence and ImpactSpecies of Alternaria have been reported worldwide on poinsettia (Table 1). Theappearance of the disease is inconsistent, however, and its impact on poinsettiaproduction is not high in most greenhouses.

2.1.2 Symptoms/SignsAlternaria leaf spot causes symptoms that are sometimes similar to other foliardiseases of poinsettia, including Phytophthora blight, bacterial canker, and scab.Lesions form on bracts, leaves, petioles, and stems. Purplish-black spots (initially0.5 mm in diameter) grow to an elliptical shape (2�4 � 4�7 mm); eventually theybecome irregularly shaped and turn brown, reaching up to 20 mm in diameter(Fig. 1). Chlorotic halos often surround lesions (Fig. 2), with leaf abscission com-mon in severe infections. Lesions on leaf veins lead to distortion. Tan to brown stemlesions (3� 8 mm) are elongated and sunken. Infection of cyathia has been reported(Yoshimura et al. 1986).

2.1.3 Biology and EpidemiologyIn Florida and other subtropical regions that experience significant rainfall, thedisease is most severe on poinsettia crops produced in shade houses or in the

Diseases of Poinsettia 3

Fig. 1 Alternaria spots mayoccur on bracts as well asleaves

Fig. 2 Alternaria leaf spotsoften show yellow haloes

Table 1 Alternaria species reported on poinsettia worldwide (Farr and Rossman 2015)

Alternaria species Location

Alternaria alternata (syn. A. tenuis) Japan, New Caledonia

Alternaria biproliformis (syn. A. heveae) China

Alternaria euphorbiae Hawaii

Alternaria euphoribiicola Florida, Hawaii, Hong Kong

Alternaria obtecta California, Louisiana

Alternaria pipionipisi, A. rostellata California

A. pseudorostrata California, United States

A. protenta (syn. A. pulcherrimae) Australia

Alternaria sp. Michigan, Tanzania, Venezuela

Alternaria tenuissima Hong Kong


landscape. The disease is rarely a problem in greenhouses, where the foliage can bekept dry through careful environmental regulation, especially with the advent of ebb-and-flood or flood-floor production, common for this crop today in many countries.

2.1.4 ManagementCultural practices that eliminate or minimize leaf wetness help limit development ofAlternaria leaf spot. Diseased plants and fallen leaf debris should be removedfrequently from the growing area.

Thiophanate-methyl should not be used for this disease as it has been shown toincrease severity of Alternaria leaf spot on some floricultural crops. Iprodione(FRAC 2), triflumizole (FRAC 3), chlorothalonil (FRAC M5), and trifloxystrobin(FRAC 11) provided about 70 % control in Florida trials, but the best control wasseen with fludioxonil (FRAC 12), azoxystrobin (FRAC 11), and mancozeb (FRACM3) (McGovern 1999; McGovern and Wilfret 1998b; McGovern et al. 2001).

Poinsettia cultivars that are relatively resistant to Alternaria leaf spot should begrown. Susceptibility varies among poinsettia cultivars; the only available reportsare from cultivars available in the 1980s–1990s. Poinsettia cultivars that are rela-tively resistant to Alternaria leaf spot should be grown. The most susceptiblecultivars included some V-14 cultivars (Glory, White, and Jingle Bells) andEckespoint C-1 Red. V-10 Amy had intermediate susceptibility. Annette Hegg(Dark Red, Top White, Brilliant Diamond, and Hot Pink) developed only tiny leafspots with tan centers in resistance trials (Engelhard and Schubert 1985). McGovernand Wilfret (1998a, 1999) reported that the poinsettia cvs. consistently least suscep-tible to Alternaria leaf spot included Freedom White, Pearl, Petoy, Sonora Pink,Spotlight Dark Red, and Subjibi.

2.2 Amphobotrys Blight [Amphobotrys ricini (Buchw.) Hennebert(syn. Botryotinia ricini (Godfrey) Whetzel)]

2.2.1 Geographic Occurrence and ImpactAmphobotrys blight and stem rot on poinsettia were first reported from Louisianaand Florida in 1988 and were noted in Bermuda in 1995 (McGovern, personalcommunication). In 2000, the same pathogen was reported from Florida attackinganother species of Euphorbia (E. milii) causing a flower blight (McMillan et al.2000). This disease appears to be regional and very rare.

2.2.2 Symptoms/SignsA foliar blight and shoot blight occur; mycelial webbing forms rapidly. Basal stemrot characterized by a soft, watery rot starting at the soil line has also been reported.The rot results in wilting without extensive stem or root rot (Holcomb and Brown1990). Small, black sclerotia have been found in infected poinsettia stems.


2.2.3 Biology and EpidemiologySeveral species in the genus Euphorbia, as well as Ricinus communis (castor bean),are susceptible to this pathogen: E. supina Raf. ex Boiss., E. heterophylla L., andE. hirta L. as well as E. pulcherrima.

2.2.4 ManagementShoot tip infections were controlled by used of a thermal fog formulation ofchlorothalonil (FRAC M5) but this did not control rot at the stem base (Holcomband Brown 1990).

2.3 Anthracnose [Colletotrichum truncatum (Schwein.) Andrusand W. D. Moore (syn. C. capsici (Sydow) E. J. Butlerand Bisby)]

2.3.1 Geographic Occurrence and ImpactAnthracnose on poinsettia caused by C. capsici (syn. C. truncatum) was reportedfrom Florida and Japan (Sato et al. 2015). Additionally, C. gloeosporioides has beenreported fromMexico, Florida, and Texas. Anthracnose on poinsettia is not commonin the United States.

2.3.2 Symptoms/SignsLeaf and stem spot and blight on poinsettia cultivar Angelika were found in agreenhouse in Japan in 2004. Brown spots 3–5 mm in diameter appeared at firston lower leaves and then enlarged along veins or leaf margins. The spots developedpale brown centers with dark brown borders and dead areas eventually dropped off.Stems became brittle as elongated lesions developed on them. Black acervuli withsetae were produced on the lesions under high humidity. Wounded andnon-wounded poinsettia plants (cv. Angelika) were inoculated, but symptoms devel-oped only on the wounded plants, 11–21 days after inoculation (Sato et al. 2008).

2.3.3 ManagementUtilize environmental control to minimize periods of wetness on leaves and bracts ofpoinsettias. Avoid wounding foliage or bracts, which might provide entry points forthe fungus.

2.4 Botrytis Blight or Gray Mold [Botrytis cinerea (syn. Botryotiniafuckeliana (de Bary) Whetz)]

2.4.1 Geographic Occurrence and ImpactBotrytis cinerea is a ubiquitous fungus. Botrytis blight occurs wherever poinsettiasare grown and causes losses in propagation, finishing, and post-harvest stages.


2.4.2 Symptoms/SignsBotrytis blight is particularly feared as a disease of bracts, but may attack allaboveground portions of poinsettia plants: stems, leaves, bracts, and flowers. Leaflesions are typically large, light to medium brown, and enlarge further with eachperiod of high humidity, sometimes creating zonate lesions. Infections often start assmall light brown lesions at the edge of bracts and grow into large wedges, havingbegun as infections at the perimeter of the leaf or bract (Figs. 3 and 4). Stem cankersare usually light brown to tan and may girdle main stems or side branches, causingwilt (Fig. 5). Flower parts may also be infected. The long brown conidiophorestopped by clumps of hyaline spores form conspicuous masses on dead plant tissue togive the disease its common name: gray mold.

2.4.3 Biology and EpidemiologyThere are hundreds of host plants for Botrytis cinerea, but poinsettia is one of themost susceptible flower crops. The pathogen is a necrotroph, growing in moribund

Fig. 3 Botrytis leaf spotsoften form wedges at the edgeof the leaf

Fig. 4 Closeup of Botrytislesion at leaf tip


tissue and secreting cell wall-degrading enzymes in advance of its hyphae. Its abilityto infect plants from a morsel of infected tissue is 200 times greater than its ability tocause infection via conidia (Sirjusingh et al. 1996). Wounds in leaves are a commonsite of infection, especially for cuttings during shipment and propagation.

Disease spread in the greenhouse is largely by dispersal of conidia by air currents(Jarvis 1980). The epidemiology of Botrytis populations has been more closelystudied in crops other than poinsettia. Conidial germination is best at 20–25 �C/68–77 �F (Blakeman 1980) in the presence of free water (Strider and Jones 1985),although germination has also been noted at extremely high humidity under labora-tory conditions. Germination may be delayed for at least 3 weeks (Salinas et al.1989) when conditions are not sufficiently moist.

Nutrients on the surface of plants are beneficial for infection, which may explainwhy wounded tissues and flower parts are more likely to be infected than intactleaves (Blakeman 1975). Applications of glucose at 0.1 M and 0.05 MKH2PO4 werefound to increase germination and infection (Kulek and Floryszak-Wieczorek 2002).Older, more mature leaves are the most susceptible of the intact foliage (Elad andEvensen 1995). Latent infections by B. cinerea are one of the main reasons why thedisease is so important as a post-harvest problem: symptoms often develop afterpoinsettias are packed and shipped (Jarvis 1977; Pritchard et al. 1996).

Bract-edge burn in poinsettias, which develops as a result of calcium deficiency atthe end of production in certain cultivars, can predispose bracts to Botrytis infectionthat destroys a plant’s salability (Barrett et al. 1995).

Inverting the day/night temperature for a poinsettia crop so that night tempera-tures were warmer than day for the purpose of producing compact plants was shownnot to affect poinsettias’ susceptibility to Botrytis blight (Pritchard et al. 1996).Higher finishing temperatures, either day or night, did increase blighting andsporulation.

2.4.4 ManagementManagement of Botrytis blight in greenhouses requires an integrated strategy, asdescribed by Hausbeck and Moorman (1996), comprised of sanitation,

Fig. 5 Botrytis stem cankersare tan in color; affectedportions of plants will wilt


environmental control, and appropriate use of fungicides. The cutting wounds madeon stock plants and the wounds on the cuttings themselves create critical controlpoints for Botrytis blight management. Poinsettia susceptibility has been shown toincrease with plant maturity (Pritchard et al. 1996), which increases the need forcareful management just when growers are concerned with shipping. Injury to bractsquickly destroys crop value.

Cultural and environmental controls are extremely important to avoid Botrytislosses in poinsettia culture. Organic debris removal from the greenhouse eliminates asource of conidial inoculum, as B. cinerea often sporulates profusely when living asa saprophyte on dead plant material. Poinsettias should be grown with adequatenitrogen and light to prevent senescence of lower leaves that could provide asubstrate for Botrytis. Avoiding the presence of free moisture is largely accomplishedby irrigation early in the day and nighttime humidity control. To prevent condensa-tion on plant surfaces, ventilation to remove warm humid air and adequate spacingbetween plants is necessary. Air movement up between plants is facilitated by a wire-mesh bench, while, in a solid-bench or tray system, horizontal air flow may beemployed to provide the necessary air movement (Augsburger and Powell 1986).

When considering nutrient effects on Botrytis blight, it is critical to avoid calciumdeficiency. Calcium can reduce the effects of B. cinerea on roses (Volpin and Elad1991). On poinsettias, calcium is an essential nutrient to prevent bract-edge burn,which provides a pathway for the initiation of Botrytis lesions on bracts. See chapter“▶Nutritional Disorders of Florists’ Crops,” for additional information.

Botrytis cinerea is notorious for developing resistance to systemic fungicides.Resistance to benomyl and thiophanate-methyl has been known in greenhousepopulations of B. cinerea for some time (Maude 1980; Moorman and Lease 1992).Resistance to dicarboximides is known (Pappas 1982; Yourman and Jeffers 1999),and fenhexamid resistance has also been noted in a US greenhouse (Moorman et al.2012).

A low-residue treatment safe for use on bracts is desired by poinsettia growers,but many fungicides specifically prohibit use on poinsettias after bract development.Treatments with thermal dusts of the fungicide chlorothalonil have been used in thepast to protect poinsettias at the end of a crop – but with the negative effect of bractfading noted in some cultivars (Powell 1977). In one study, injury to bracts with athermal dust treatment of chlorothalonil was found on more cultivars grown with a24 �C/75 �F night temperature than with at 21 �C/70 �F night temperature (Carlsonand Emino 1969). Current labels in the United States indicate that a chlorothalonilthermal dust is to be used on poinsettias prior to bract formation only. The greatestreduction in disease severity was seen with fenhexamid and pyraclostrobin +boscalid treatment in a trial on poinsettias in bract (Leonberger and Beckerman2009). Prior to bract coloration, a large number of active ingredients are available foruse against Botrytis blight on poinsettias in the United States: chlorothalonil (FRACM5), mancozeb (M3), coppers (FRAC M1), fludioxonil (FRAC 12), cyprodinil +fludioxonil (FRAC 9 + FRAC 12), fenhexamid (FRAC 17), iprodione (FRAC 2),polyoxin D (FRAC 19), pyraclostrobin + boscalid (FRAC 11 + 7), and strobilurins(FRAC 11). Biofungicides labeled in the United States for Botrytis management


http://link.springer.com/Nutritional Disorders of Florists’ Crops

include Bacillus subtilis (FRAC NC), Streptomyces spp. (FRAC NC), andReynoutria sachalinensis extract (FRAC P). Studies have shown the effectivenessof newer fungicides (Hausbeck and Harlan 2012), including fenhexamid (Bensonand Parker 1999) and strobilurin materials (Benson and Parker 2000a, 2000b), onpoinsettia against Botrytis blight.

Genetic control is also relevant for Botrytis blight on poinsettias. Cultivars grownin the 1970s varied in susceptibility to the disease (Shanks 1972; Witte and Miller1976; Manning et al. 1972). Since cultivars grown today are different from those inthe 1970s, more recent cultivar comparisons would have more practical value. Eladand Evensen (1995) discussed the various processes associated with senescence thatcould inform the approach to breeding for resistance to B. cinerea in its many hosts.They suggested various techniques for thwarting senescence effects such asincreased membrane permeability, including increasing the antioxidant systemsand reducing the ethylene response. Physical barriers could also be optimized bydeveloping a thicker, more hydrophobic cuticle, or providing inhibitors of cutinase.Giving poinsettias new defenses against cell wall-degrading enzymes or increasingthe wound response rate would be additional strategies. Keeping latent infectionsquiescent longer and increasing the expression of various chemical defenses areadditional goals that would result in improved poinsettia resistance to Botrytis blight.

Learning how to stimulate natural plant resistance mechanisms may provide newavenues of management for B. cinerea on poinsettias in the future. Systemicacquired resistance effects were obtained in poinsettia with benzothiadiazole(BTH): treatments at 0.3 mM decreased the susceptibility of ‘Coco White’ and‘Malibu Red’ poinsettia cultivars in a leaf-disc assay (Kulek and Floryszak-Wieczorek 2002).

2.5 Choanephora Wet Rot [Choanephora cucurbitarum (Berk.and Rav.) Thaxter]

2.5.1 Geographic Occurrence and ImpactChoanephora cucurbitarum causes a soft, wet rot of poinsettias. The disease usuallyoccurs at the hottest times (August through October) and may affect plants at allstages of production.

2.5.2 Symptoms/SignsSymptoms of Choanephora wet rot resemble those caused by Rhizopus stolonifer. Asoft, mushy decay can develop on infected leaves and petioles. Infected stems wiltprior to collapsing. Young plants are destroyed under humid conditions, while olderplants may develop only a few branches with symptoms. C. cucurbitarum producescharacteristic whisker-like sporangiophores on diseased tissues (Engelhard 1987).

2.5.3 Biology and EpidemiologyC. cucurbitarum also causes rot of fruits and vegetables as well as blighting of flowersand, in some cases, immature stems of Hibiscus rosa-sinensis and Petunia � hybrida.


Disease develops very rapidly under warm to hot, humid to wet conditions. On bellpepper and swamp Hibiscus, the fungus ceases sporulation at temperatures above14 �C/57 �F.

2.5.4 ManagementMinimizing plant stress and spacing to promote air circulation and minimizing leafwetness have been suggested for management of this disease. Excellent control ofwet rot on poinsettia has been reported with azoxystrobin (FRAC 11), copperpentahydrate (FRAC M1), and chlorothalonil (FRAC M5) (McGovern 1999).

2.6 Corynespora Leaf and Bract Spot [C. cassiicola (Berk. and M.A. Curtis) C. T. Wei (syn. Helminthosporium cassiicola Berk.and M. A. Curtis)]

2.6.1 Geographic Occurrence and ImpactCorynespora leaf and bract spot on poinsettia was first reported from Florida (Chaseand Simone 1986) and Louisiana (Holcomb and Fuller 1993). The disease hasappeared only rarely in the past 20 years.

2.6.2 SymptomsOn poinsettia, large, irregularly shaped, brown to black lesions form on bracts andleaves and strongly resemble those caused by Botrytis cinerea infections (Fig. 6).They occur primarily at the tips and margins of leaves and may be as large as 3 cm indiameter. In some cases disease is more prevalent on immature plants.

2.6.3 Biology and EpidemiologyWounding is not usually necessary for infection on poinsettia. C. cassiicola is spreadby airborne spores. High moisture and humidity are conducive to infection. Thefungus has been observed to survive on plant debris for 2 years. Lesions developwithin 10 days of infection. Most isolates show no host specialization. A variety ofplants are hosts for C. cassiicola, including Aeschynanthus pulcher (lipstick vine),Aphelandra squarrosa (zebra plant), Catharanthus roseus (annual vinca), Hydran-gea macrophylla, Saintpaulia ionantha (African violet), and Salvia splendens (scar-let sage), as well as vegetable and field crops.

2.6.4 ManagementReduction of humidity and leaf wetness duration are important for preventinginfection. Fungicide trials on hydrangeas indicate excellent control withazoxystrobin (FRAC 11), triforine (FRAC 3), copper products (FRAC M1), and apremix of propiconazole and chlorothalonil (FRAC 3 and M5).


2.7 Fusarium Stem Rot [Fusarium solani (Mart.) Sacco]

2.7.1 Geographic Occurrence and ImpactFusarium stem rot was reported from Wisconsin in 1987 (Heimann and Worf 1987).No additional research and few reports are available: the disease is apparently rare.

2.7.2 SymptomsBasal cankers, usually about 2 cm above the soil line and 3–6 cm long, are formed(Fig. 7). Lesions noted in Wisconsin were brown to black, somewhat shrunken, andhad distinct necrotic margins. All stem tissues except the pith were affected andsometimes the bark tissue appeared shredded. Although cankers became obviousafter potting, infected plants developed normally. Stress in the retail environment didresult in wilting on retail shelves.

2.7.3 ManagementSymptom similarity with Rhizoctonia stem rot may cause misidentification by plantproducers. Fungicides for prevention of Rhizoctonia stem rot fortunately could beexpected to prevent Fusarium stem rot as well.

2.8 Powdery Mildews: Leveillula clavata Nour, L. taurica (Lev.)G. Arnaud, Pseudoidium poinsettiae (U. Braun, Minnis,and Yañez-Morales), Phyllactinia poinsettiae, andOvulariopsiserysiphoides

2.8.1 Geographic Occurrence and ImpactSee Table 2 for reports of occurrence.

The greatest impact of a powdery mildew on poinsettia has been seen fromPseudoidium poinsettiae (sometimes referred to as Oidium poinsettiae) affectingplants in the United States, Mexico, Puerto Rico, and Europe. The disease was firstseen in the United States in 1990 in Pennsylvania and the Pacific Northwest

Fig. 6 Corynespora leaf andbract spot on transitionalbracts


(Daughtrey and Hall 1992; Kim and Olson 1994); crops in Mexico and Puerto Ricowere affected by the disease at about the same time (Daughtrey and Hall 1992). Thedisease appeared in numerous other states in subsequent years. The mildew seen inthe United States has also been seen in the United Kingdom and Europe (Denmark,Germany, and Sweden) starting with the appearance of the Pseudoidium in Denmarkin 2005 (Anonymous 2002). The impact of this powdery mildew comes not from itseffect on plant health, but from the visibility of the fungus: the aesthetic quality of thecrop plummets immediately, and infected plants are not saleable. In addition, ifpoinsettias are sold that have unnoticed infections, the disease will continue todevelop in homes and interiorscapes, resulting in obvious white spotting on coloredbracts that leads to immense customer dissatisfaction. After the initial few years inwhich the disease was seen in the poinsettia production industry, when manygrowers experienced total crop failures, incidence has been sporadic and economiclosses have been much less severe. This is due to vigilant scouting and judicious

Table 2 Powdery mildew reports on poinsettia from around the world (Farr and Rossman 2015;Siahaan et al. 2015; Daughtrey and Hall 1992; Anonymous 2002)

Powdery mildew species Location

Leveillula clavata Canary Islands, Italy, India, Indonesia,Kenya, Tanzania

Leveillula taurica syn. Oidiopsis taurica Canary Islands, Tanzania, India, Indonesia,Kenya

Leveillula sp. Israel

Oidium sp. El Salvador, Ethiopia, Guatemala, Mexico,United States

Ovulariopsis erysiphoides Venezuela

Pseudoidium poinsettiae (syn. Oidiumpoinsettiae), Erysiphe poinsettiae

Mexico, Puerto Rico, Denmark, Germany,Sweden, United States

Phyllactinia poinsettiae Indonesia

Fig. 7 Fusarium cankers arebrown and form at the soil line


applications of protective fungicide at all levels of production. This powdery mildewcontinues to be found in a few greenhouses in North America almost every year.

2.8.2 Symptoms/SignsPowdery mildew caused by Pseudoidium poinsettiae can be difficult to scout forduring the spring and summer, as there are no white colonies then on the upper leafsurface: the only symptoms may be a few round, diffuse, chlorotic spots on theleaves (Fig. 8). Beneath these pale areas, on the abaxial side of the leaf, there aresparse, often indistinct, powdery mildew colonies (Fig. 9). In the fall, when green-house temperatures cool, conspicuous white colonies develop on the upper surfaceof leaves and bracts (Fig. 10). When oval to cylindrical conidia are produced (singly,but forming false chains) from the surface mycelium, the colonies take on a moregranulated (“sugar-coated”) appearance. If the growth of the powdery mildew isunchecked by fungicide application, colonies will grow until they merge and coverthe surface of leaves or bracts.

Fig. 8 Powdery mildewcauses chlorotic spots on theupper leaf surface, whichmark the location of colonieson the undersurface

Fig. 9 Powdery mildewcolonies appear first on theleaf undersurface


Powdery mildew symptoms caused by Leveillula clavata (syn. Oidiopsis taurica)as described from a 2005 appearance in Italy (Garibaldi et al. 2006) are similar tothose in early (summer) infections of poinsettia by Pseudoidium poinsettiae in theUnited States – both fungi cause yellow spots on adaxial leaf surfaces. In otherrespects the disease caused by L. clavata is quite different: bract infections have notbeen reported with L. clavata. Club-shaped conidia are borne singly on conidio-phores that emerge through stomates on the abaxial leaf surface, where a rose toreddish mycelium also appears. Chasmothecia with a hemispherical, lenticular orpezizoid shape and simple appendages, containing many asci each with two asco-spores, were described on poinsettias in Kenya (Nour 1957). A similar powderymildew fungus has also been reported on poinsettia from Japan (Horie et al. 2006).

A third genus of powdery mildew, Phyllactinia poinsettiae (syn. Ovulariopsispoinsettiae), was recently reported from Indonesia (Siahaan et al. 2015). Thismildew forms subevanescent colonies on the abaxial side of leaves. Club-shapedconidia with papillate tips are produced singly on conidiophores arising fromhyphae.

2.8.3 Biology and EpidemiologyStudies of powdery mildew management on poinsettia have largely been confined toPseudoidium poinsettiae (syn. Erysiphe poinsettiae). Studies at Michigan StateUniversity on this fungus showed conidial germ tubes appearing on poinsettia‘Freedom Red’ at 2 h post-inoculation (Celio and Hausbeck 1998); germinationreached a peak at 36 h. Appressoria were slightly lobed to lobed. Over half of thegerminated conidia had established a globose haustorium within 48 h. Basal cells ofconidiophores were arced distinctively. Early steps in colony establishment (per-centage of conidial germination, secondary germ tube formation, and haustoriumformation) were limited at 30 �C/86 �F as compared to 20 �C/68 �F. The powderymildew can be maintained on symptomless plants over the summer (Kim et al.1995a), thus growers should not count on disease eradication through exposure totypical summer greenhouse temperatures. The suppressive effect of high tempera-tures on powdery mildew of poinsettia is, however, reflected in field observations

Fig. 10 Bracts as well asleaves are susceptible topowdery mildew


that the disease does not progress during the summer months in the northeasternUnited States (Kim et al. 1995a). The optimum for germination of conidia was foundto be 25 �C/77 �F and 85 % relative humidity (RH) in greenhouse studies (Hausbeckand Kalishek 1994), conditions which are typically available in greenhouses intemperate climates in the fall.

Peak concentrations of conidia in the greenhouse were associated with dips in RHor changes in temperature, which often occurred simultaneously (Shaw andHausbeck 1995; Byrne et al. 2000). Symptoms were more severe and the conidialconcentration was higher (1,221 conidia/m3 air/h) in one greenhouse with an averageRH of 64 %, while the conidial concentration in a similar greenhouse with anaverage RH of 53 % was only 317 conidia/m3 air/h.

Studies in Germany indicated that the powdery mildew from poinsettia (referredto as Oidium sp. but presumably the Pseudoidium seen in the United States at aboutthe same time) could be transferred to other Euphorbia spp. as well E. exigua,E. heterophylla, E. helioscopia, and E. marginata (Anonymous 2004). These plantsor wild E. pulcherrima could provide a reservoir of inoculum near poinsettia cuttingproduction facilities.

2.8.4 Management• Cultural practices – Keeping humidity down (<85 %) in the greenhouse and

improving air circulation help to slow an epidemic of powdery mildew, but arenot sufficient to halt it (Hausbeck and Kalishek 1994). The disease continues todevelop after poinsettias leave the greenhouse and enter retail or customerenvironments. Treatment with elevated temperature (>30 �C/86 �F) has beensuggested as a possible technique for specialist propagators to use prior toshipping cuttings (Celio and Hausbeck 1998), but the plant safety and effective-ness of this procedure have not yet been tested.

• Sanitation – Fortunately P. poinsettiae has not been found causing disease on anyother hosts in northern temperate climates, so removing all poinsettias from thegreenhouse at the end of the growing season is likely to provide completeeradication of inoculum. Inadvertent reintroduction on cuttings the next seasonis the grower’s only concern unless plants are being grown in subtropical areaswhere poinsettias grow year-round. Removing infected leaves as soon as they aredetected is not often a practical solution, but reduces inoculum in the greenhouseand at high greenhouse temperatures could be eradicative early in the growingseason (Hausbeck et al. 1994). Early detection of powdery mildew is important,as it alerts the grower to the need for an appropriate fungicide program for thatyear’s crop. Leaf removal must be combined with fungicide treatment to avoidextensive crop loss in the fall, when greenhouse conditions become more condu-cive to disease development and spread. Chasmothecia have not been found forP. poinsettiae, thus there is no persistent inoculum on leaf debris in the green-house after plants are sold.

• Fungicides and biocontrols – Fungicides have been very effective against thePseudoidium on poinsettia, perhaps in part because the fungus was introduced tohorticultural productions systems only recently. Both protectant and systemic


materials have been very effective when used preventively. Sprays for powderymildew control need not be applied unless the pathogen is present, so a carefulscouting program should be in place in order to detect the disease before it iswidespread. Many fungicide labels restrict use on poinsettias to the time beforebracts begin to color, so chemical control must be established before the finishingstages. Weekly or biweekly treatments of a wide range of materials includingpotassium bicarbonate (FRAC NC), copper pentahydrate (FRAC M1),thiophanate-methyl (FRAC 1), trifloxystrobin (FRAC 11), kresoxim-methyl(FRAC 11), polyoxin D (FRAC 19), pyraclostrobin (FRAC 11), iprodione(FRAC 2), and demethylation inhibitor materials (triflumizole, triadimefon, andmyclobutanil) (FRAC 3) have provided significant protection (Daughtrey andMacksel 1995; Daughtrey and Tobiasz 1999; Gould and Bergen 1995a, b;Hausbeck and Kusnier 1995a, b, c, 1996; Hausbeck et al. 2002a, b; Daughtreyand Tobiasz 2009). Rotation of active ingredients with different modes of actionis essential for powdery mildew management, so it is fortunate that there are manyfungicide options for this purpose during all but the finishing stages ofproduction.Biological controls are desirable for powdery mildew control in poinsettias,particularly because growers are not comfortable applying fungicides to coloredbracts and because many fungicide labels prohibit such use. A program alternat-ing a biological control (Bacillus subtilis) with a biorational material (potassiumbicarbonate) reduced powdery mildew significantly in an inoculated trial(Daughtrey and Tobiasz 2010).

• Resistance – There is no known resistance to powdery mildew (Pseudoidiumpoinsettiae) in poinsettia, but the level of susceptibility varies among cultivars.Celio and Hausbeck (1997) tested 11 cultivars for susceptibility, and all devel-oped powdery mildew colonies within 31 days. Three red cultivars tested hadsignificantly more powdery mildew than other cultivars in two trials. Kim et al.(1995b) reported higher susceptibility in leaves and bracts of the cultivar ‘Free-dom Red’ as compared to the older cultivars ‘Dark Red Hegg’ and ‘V-17Angelika White’ in a greenhouse trial. If the most popular red cultivars areprone to powdery mildew, growers may not have the option of growing lesssusceptible types. Prioritized scouting of the more susceptible red cultivars hasbeen suggested (Celio and Hausbeck 1997) to improve scouting efficiency. In atrial in Germany, Euphorbia fulgens and E. milii were not infected with thepathogen although four other Euphorbia species were shown to be hosts (Anon-ymous 2004). Plant breeders will ideally expose prospective new lines toP. poinsettiae to select for poinsettias with low susceptibility to this disease.

2.9 Pythium Root Rot (Pythium spp.)

2.9.1 Geographic Occurrence and ImpactPythium species are water molds belonging to the Oomycetes and not true fungi. Thespecies reported to occur on poinsettia are P. aphanidermatum, P. cryptoirregulare(syn. Globisporangium cryptoirregulare), P. debaryanum (syn. Globisporangium


debaryanum), P. irregulare (syn. Globisporangium irregulare), P. perniciosum, andP. ultimum (Farr and Rossman 2015) as well as P. myriotylum and P. helicoides(Miyake et al. 2014). Strider and Jones (1985) mention P. ultimum as the primaryproblem in poinsettia production up until that time, but P. aphanidermatum hascaused the most dramatic losses in recent years (Moorman et al. 2002).

Pythium root rot is widely distributed, and no doubt occurs wherever this crop isgrown. Formal reports of Pythium root rot on poinsettia caused by one or morespecies have come from South America, the United States, Japan, New Zealand, andBrazil (Farr and Rossman 2015). The disease can have imperceptible effects on plantquality or can cause extensive mortality of poinsettias, especially in irrigationsystems that allow recirculation of water. The particular Pythium species that areimportant today are different from those that were important in the first half of thetwentieth century, largely due to a shift to production systems using soilless mediaand recirculating subirrigation. Changes in the cultivars grown may also haveaffected which root diseases are most important, and production of cuttings in newgeographic areas around the world may have led to the introduction of new pathogenspecies or strains.

2.9.2 Symptoms/SignsThere is a soft brown or gray-brown rot of the cortex of the fibrous roots, whichcontrasts sharply with the white, vigorous growth of a healthy root system (Fig. 11).Severe aboveground symptoms of Pythium root rot include stunting of the wholeplant and even wilting and death. Leaves yellow, starting with the lower leaves, andmay curl upward as they wilt. In advanced infections, the cortex will slough off thehard xylem core as the plant is pulled from the pot, leaving behind thin white stringsof xylem (Fig. 12). Symptoms appear on the roots on the outside of a rooting cube oron roots adjacent to pot sidewalls; they are generally most pronounced in the bottomof the pot. Because Thielaviopsis basicola and Rhizoctonia solani both cause a drierlooking rot, Pythium root rot is most easily confused with Phytophthora or Fusarium

Fig. 11 Pythium root rot (atright) in contrast to a healthyroot system


root rots. Fungus gnat feeding is often coincident with Pythium root rot, but eitherthe insect or the water mold acting alone can cause serious root injury. See chapter“▶ Insect Management for Disease Control in Florists’ Crops,” for additionalinformation.

2.9.3 Biology and EpidemiologyThe biology of the different Pythium species varies somewhat, but there are charac-teristics that they share. They are fungus-like in their appearance, but molecularstudies have verified the longtime suspicion that they are members of a uniquegroup, more closely related to algae than to fungi. Pythium spp. possess coenocytichyphae with cell walls composed of cellulose rather than the chitin of a true fungus.In the wet environments that are favorable for infection, most Pythium speciesaccomplish asexual reproduction by forming sporangia (in some cases these aremerely swollen hyphae). Motile zoospores are released from thin-walled vesiclesproduced by the sporangium of a Pythium sp., rather than being formed within thesporangium in the manner of Phytophthora. Often chlamydospores and/or hyphalswellings may be formed by the hyphae as well.

The sexual structures are termed oogonia and antheridia, with these structuressometimes coming from the same individual and sometimes requiring an oppositemating type. The result of fertilization of an oogonium by one or more antheridiaresults in the formation of an oospore. The thick walls of the oospore make it veryresistant to environmental stresses and to other microorganisms, so it is a long-termsurvival structure. Oospores in organic debris are the main source of contaminationin a greenhouse operation. Oospores are sometimes present in the peat moss itself orsometimes linger in recycled pots or trays that have not been thoroughly cleaned anddisinfested. Morphological differences were originally used to identify Pythiumspecies, but DNA analysis has led to many changes in Pythium taxonomy andnomenclature in recent years, including the creation of new genera that were onceconsidered to be within the genus Pythium (Uzuhashi et al. 2010).

Because different Pythium species have different temperature optima, problemswith particular species may appear at different times of year. The most commonly

Fig. 12 Pythium root rot(showing xylem remainingafter cortex has sloughed off)


http://link.springer.com/Insect Management for Disease Control in Florists’ Crops

encountered Pythium in earlier years, when poinsettias were grown in soil-basedmedia, was P. ultimum; root rot from this pathogen was shown to be most severe at17 �C/62 �F and to cause little effect at temperatures at or above 26 �C/79 �F(Bateman and Dimock 1959). Pythium root rot was at that time seen commonly atthe end of the production season, when temperatures were lowered to slow plantdevelopment prior to sale.

Today, P. ultimum is occasionally encountered, but the most serious Pythiumpathogen on poinsettia in North America today is Pythium aphanidermatum, firstseen in 1977 as a pathogen on poinsettia in Canada on plants grown from cuttingspropagated in the United States (Moorman et al. 2002; Komorowska-Jedrys et al.2008). This organism causes disease at higher temperatures than P. ultimum(Hendrix and Campbell 1973) and produces prolific numbers of zoospores thatmake it ideally suited to thrive in recirculating irrigation systems (Sanogo andMoorman 1993). Temperatures are favorable to P. aphanidermatum in summer,when most of the vegetative growth of poinsettias takes place. This species wasreported causing cutting rot in soilless production systems in Brazil (Palmucci andGrijalba 2007). In addition, Miyake et al. (2014) reported sudden outbreaks of rootrot in ebb-and-flood production of poinsettias in Japan, with P. myriotylum andP. helicoides discovered to be the pathogens. Their subsequent research found thatisolates of all three high-temperature-loving Pythium species – P. aphanidermatum,P. myriotylum, and P. helicoides – gave the greatest incidence and severity of root rotat 35 �C/95 �C when inoculated to poinsettia. Although favored by hot environ-ments, all three were able to cause disease at 20 �C/68 �F at higher inoculum(zoospore) levels.

Bateman (1961) found that overwatering (keeping soil at 70 % moisture holdingcapacity or above) promoted Pythium root rot in ‘Barbara Ecke’ poinsettias. He alsoshowed that neutral to alkaline soil was favorable to root rot caused by P. ultimum(Bateman 1962).

A study by Moorman (1986) showed that growing poinsettias with higher fertilityincreased Pythium root rot caused by P. ultimum. Fertilization rates tested rangedfrom 100 to 600 μg N/g. Higher soluble salt levels were correlated with increasedmortality in poinsettias inoculated with P. ultimum early in production in threedifferent soilless mixes as well as in a soil-containing mix.

2.9.4 ManagementIdentification of the species of Pythium present is important to designing a manage-ment program. Both P. irregulare and P. cryptoirregulare, indistinguishable mor-phologically, occur on poinsettias in greenhouses (Garzon et al. 2007) and are rarelyproblematic unless cultural controls are mismanaged. P. aphanidermatum,P. helicoides, and P. myriotylum are all relatively aggressive pathogens and are allfavored by high temperature. Globalization of the ornamental plant trade is no doubthaving an effect on the species and genotypes of Pythium and other pathogens thatare encountered in greenhouses. An analysis of P. aphanidermatum found onpoinsettia in Pennsylvania greenhouses noted genotypes from around the world(Lee et al. 2010). Variation in susceptibility to P. aphanidermatum among poinsettia


cultivars has been noted (Daughtrey and Hyatt 2012); growers experiencing exten-sive losses may find it worthwhile to trial different cultivars.

Poinsettia growers are generally fearful of Pythium root rot losses and use verycareful sanitation procedures and treatments with biological and chemical fungicidesto ensure crop safety. Sanitation efforts are directed against the introduction ofoospores in field soil, a particular threat in flood-floor operations. Whereas earlierproduction methods included steam pasteurization to ensure the safety of soil-containing growing media, today’s poinsettia growers use soilless growing mixesbased largely on sphagnum peat moss. Cuttings are often rooted in artificial foammaterials – a practice which eliminates peat moss as a possible source (Graham1994). Clean growing surfaces and clean irrigation and handling practices usingsoilless media provide a measure of security that was not available to a poinsettiagrower 50 years ago. Sanitation between crops will be especially important inoperations with recirculating irrigation systems, which favor dissemination andinfection of Pythium spp. Miyake et al. (2014) noted that poinsettias were firstseen with root rot caused by P. helicoides in Japan in ebb-and-flow productionfollowing rose and begonia crops that were known hosts of that species. Althoughmonitoring for Pythium root rot is usually a matter of watching for symptoms, bent-grass traps have been used to monitor for populations of high-temperature Pythiumspecies in ebb-and-flood systems in Japan. These traps successfully detected thepathogens 30 days before symptom development was evident from infections ofP. helicoides in potted miniature roses (Watanabe et al. 2008).

Boehm and Hoitink (1992) found that higher microbial activity in a light-colored,less-decomposed sphagnum peat was associated with short-term suppression ofPythium root rot. Treatments with bioantagonists against P. ultimum var. ultimumin subirrigated poinsettias were trialed in Canada (Little et al. 2003). Quality wassimilar when inoculated plants were protected with metalaxyl or with treatments ofStreptomyces griseoviridis strain K61 or S. lydicus strain WYEC 108. Otherbioantagonist products including Trichoderma spp. and Bacillus subtilis activeingredients are also labeled for use against Pythium spp. in greenhouses.

There are few fungicides with strong effectiveness against Pythium. Trials haveshown the relative effectiveness of some of the oomycete fungicides (Parker andBenson 2011, 2012, 2013; Benson and Parker 2001b; Hausbeck and Harlan 2007).Fungicides that have been used for Pythium management include metalaxyl/mefenoxam (FRAC 4), the effectiveness of which has been reduced in the green-house arena due to the development of resistance in some Pythium populations(Moorman et al. 2002). The effectiveness of etridiazole (FRAC 14), sold singly andalso in combination with thiophanate-methyl (FRAC 1) for broad-spectrum root rotmanagement, continues: there has not been any resistance to this active ingredient ingreenhouse Pythium populations. Fosetyl-Al and other phosphorous acid materials(FRAC 33) can reduce Pythium losses to some degree. More recently, cyazofamid(FRAC 21) and fluopicolide (FRAC 43) have been introduced for control of Pythiumroot rot in greenhouses. Strobilurins (FRAC 11) give partial but not strong control ofPythium.


2.10 Phytophthora Crown and Root Rot (Phytophthora drechsleri,P. nicotianae, P. cryptogea)

2.10.1 Geographic Occurrence and ImpactThree species of Phytophthora have been reported from poinsettia: P. drechsleri(Korea and the United States) and P. nicotianae (United States, Korea, Brazil, PuertoRico, Japan) have been known to be poinsettia pathogens for some time (Farr andRossman 2015; Kanto et al. 2007; Estevez de Jensen et al. 2006). In Taiwan,P. cryptogea as well as P. nicotianae occurred on rotted poinsettia roots (Ann1992), and Orlikowski also described P. cryptogea on poinsettia in Poland(Orlikowski and Ptaszek 2013). Some additional species have been seen on Euphor-bia relatives of poinsettia, including P. cactorum, P. citricola, and P. palmivora. Thedisease is lethal to infected plants. Its impact depends upon the production system: ingreenhouses with recirculating irrigation systems, the potential for extensive croploss is high. Poinsettia cultivars vary in their susceptibility to Phytophthora root rot(Woodworth and Hausbeck 2003).

2.10.2 Symptoms/SignsThe part of the poinsettia plant affected by Phytophthora varies from outbreak tooutbreak: whereas Engelhard and Ploetz (1979) described P. nicotianae causing acrown and stem rot, in Hawaii a short time later, P. nicotianae and P. drechsleri werefound causing symptoms on leaves, cyathia, and bracts (Yoshimura et al. 1985). Inthe United States, P. drechsleri has been a significant problem in cutting productionin ebb-and-flood benches, causing root rot and stem rot (Lamour et al. 2003)(Fig. 13). P. cryptogea caused extensive stem base rot as well as root rot and wilton stunted poinsettias in an outbreak in Poland (Orlikowski and Ptaszek 2013).

2.10.3 Biology and EpidemiologyThe pathogen is thought to be moved from greenhouse to greenhouse on cuttings(Lamour et al. 2003). Infected stock plants may lead to extensive loss of cuttingsduring propagation. Because of the production of sporangia and zoospores, dispersal

Fig. 13 Root rot caused byPhytophthora drechsleri


of Phytophthora inoculum during production is especially likely in plants grown ona subirrigated recirculating irrigation system (Strong et al. 1997). In a US study, thepopulations of P. drechsleri affecting two poinsettia greenhouses were unique to thetwo locations and showed no genetic diversity within a greenhouse (Lamour et al.2003), indicating asexual reproduction within the two facilities.

2.10.4 ManagementRemoving the obviously diseased plants from a recirculating irrigation system is notsufficient to remove all of the inoculum when attempting to halt an epidemic. Asystem for filtering beneath each pot would be ideal (Van der Gaag et al. 2001), oralternatively treating water to be toxic to zoospores would be useful (von Broembsenand Deacon 1997). Trials have shown the benefit of certain fungicide treatments toprevent Phytophthora disease on poinsettias (Daughtrey and Tobiasz 2003;Hausbeck and Harlan 2009). Current methods in the production industry rely heavilyupon chemical control in response to an outbreak, with fungicides registered for thisuse in the United States including cyazofamid (FRAC 21), dimethomorph andmandipropamid (FRAC 40), etridiazole (FRAC 14), fluopicolide (FRAC 43),fosetyl-Al and other phosphorous acid compounds (FRAC 33), mefenoxam(FRAC 4), and strobilurins (FRAC 11) (Daughtrey et al. 2015). There is littlepublished data on the use of biopesticides for Phytophthora disease suppression inpoinsettias (Hausbeck et al. 2004a).

2.11 Rhizoctonia Cutting Rot, Crown Rot, and Root Rot[Rhizoctonia solani Kuhn (syn. Thanatephorus cucumeris(A. B. Frank) Donk)]

2.11.1 Geographic Occurrence and ImpactRhizoctonia solani is widely distributed, has a wide host range, and is very commonin propagation of poinsettias.

2.11.2 Symptoms/SignsWhen R. solani causes cutting rot, stems become darkened and mushy at the soil line(Fig. 14). Under the warm, humid conditions typical of propagation, the fungus willgrow over the rooting cube as well as the entire cutting (Fig. 15). When this occurs, alight brown mycelium, closely appressed to the plant tissues and soil, is sometimesvisible. The fungus grows out more or less radially from the point of contamination,giving the damage a circular or arc-shaped pattern. The mycelium can also cause aweb blight and appears as a brown, cobweb-like growth on the leaves. Leaves incontact with the growing medium can develop roughly circular lesions (Fig. 16).

Root rot caused by R. solani usually shows discrete, brown lesions and rotting ofthe cortical tissues, leading to decreased plant development. R. solani causes cuttingrot more often than root rot, although poinsettia is quite susceptible to Rhizoctoniaroot rot.


Crown rot commonly occurs in the absence of root rot and first appears as a browncanker at the root crown. Longitudinal cracking and a dry appearance of the rottedcrown tissues often develop on older plants. Other aboveground symptoms includechlorosis, wilting, loss of lower leaves, and in severe cases stunting and plant death.

Fig. 14 Rhizoctonia stem rot

Fig. 15 Root rot caused byRhizoctonia solani, withvisible mycelium on thesurface of rooting cubes


2.11.3 Biology and EpidemiologyPoinsettias are most susceptible just before or soon after rooting and just prior toplant maturity. R. solani generally grows best in potting media that are evenly moistand warm: Rhizoctonia root rot increases at soil temperatures between 17 and 26 �C(62 and 79 �F) (Bateman and Dimock 1959) with a moisture holding capacity below40 %. R. solani also grows best in soils with high oxygen and low carbon dioxidelevels (Bateman 1961).

2.11.4 ManagementSanitation practices to guard against soilborne fungi are applicable to R. solani.Methods for keeping field soil out of contact with a soilless growing medium areeffective at preventing most Rhizoctonia disease problems for poinsettias.

• Cultural methods – Composts from municipal sewage sludge have been exploredfor use in ornamental production. Compost cured for at least 4 months with aninternal temperature<60 �C/140 �F suppressed Pythium but not Rhizoctonia spp.An additional 4 weeks of storage resulted in a medium suppressive to Rhizoctoniaas well as Pythium. Trialing a potting medium amended with 25 % of the agedcompost showed that poinsettias had significantly less root damage caused byR. solani (Kuter et al. 1988).Suppression of Rhizoctonia crown and root rot of poinsettia was evaluated inpotting mixes prepared with dark, highly decomposed sphagnum peat; with light,less-decomposed sphagnum peat; or with composted pine bark. In none of themedia was the disease consistently suppressed. Inoculation of these mixes withChryseobacterium gleum (C299R2) and Trichoderma hamatum 382 (T382) sig-nificantly reduced the severity in the composted pine bark mix. Both biocontrolagents maintained high populations over 90 days in this medium. The microor-ganisms were less effective in the light and dark peat mixes, in which populationsof C299R2 declined. In contrast, crown and root rot was suppressed in all threetypes of mixes where high populations of T382 were maintained (Krause et al.2001).

Fig. 16 Mycelium ofRhizoctonia solani on ablighted leaf


• Biological Control – A variety of antagonists/biological control organisms havebeen evaluated for their ability to affect Rhizoctonia cutting rot on poinsettia.Cartwright and Benson (1994) evaluated the effects of Burkholderia (syn. Pseu-domonas) cepacia (strain 5.5B) and Paecilomyces lilacinus (isolate 6.2 F) appliedto polyfoam rooting cubes and found that colonization of cubes by R. solani wasreduced in cubes treated with B. cepacia. Colonization of the P. lilacinus-treatedcubes by R. solani was significantly less than colonization of infested controls.Direct treatment of poinsettia stock plants with sprays of B. cepacia was alsoeffective in preventing Rhizoctonia cutting rot (Cartwright and Benson 1995a,1995b). Survival of B. cepacia and P. lilacinus in rooting cubes showed thatP. lilacinus was stable over a 3-week period, while some strains of B. cepaciadecreased after only 7 days. The population level of these antagonists determinedthe amount of protection of poinsettia cuttings against R. solani.Strategies for applying Burkholderia cepacia (strain 5.5B) and Pesta formulationsof binucleate Rhizoctonia (BNR) isolates (BNR621 and P9023) were evaluated(Hwang and Benson 2002). B. cepacia suppressed Rhizoctonia cutting rot duringpropagation, while BNR isolates did not. After transplanting, BNR isolates weremore effective for suppression of stem and root rot than application of B. cepacia.Application of different biocontrol agents during the different production phasesof poinsettia was effective for disease control.

• Fungicides – Fungicides such as strobilurins (FRAC 11), fludioxonil (FRAC 12),iprodione (FRAC 2), pentachloronitrobenzene (FRAC 14), thiophanate-methyl(FRAC 1), and triflumizole (FRAC 3) are effective as drenches against Rhizoc-tonia. Treatments must be made before infection occurs.The effect of spraying the surface of rooting cubes compared to soaking the cubeswith the same fungicides was evaluated by Benson (1991). Surface sprays withbenomyl (FRAC 1), flutolanil (FRAC 7), iprodione (FRAC 2), or chlorothalonil(FRAC M5) prevented Rhizoctonia infection. Rooting cube soaks with benomyl,flutolanil, or iprodione were as effective as the sprays of the cubes in preventingdisease. Rooting cube soaks with benomyl and sprays with iprodione,chlorothalonil, or benomyl inhibited root initiation but not final growth of theplant. A rooting cube soak with iprodione did not affect rooting (Benson 1992).Azoxystrobin (FRAC 11) as a preplant soak to rooting cubes or post-plant spraywas also effective against R. solani and not harmful to the plant (Benson andParker 2001a).

2.12 Rhizopus Blight [R. stolonifer (Ehrenb.:Fr.) Vuill. (syn. Rhizopusnigricans Ehrenb.)]

2.12.1 Geographic Occurrence and ImpactRhizopus blight of Euphorbia spp. (including poinsettia) was reported during the1980s in Florida (Chase and Engelhard 1984). The pathogen is more commonlyknown as a bread mold or storage mold on ornamentals, soft fruits, and vegetables.


2.12.2 Symptoms/SignsTypical growing conditions in the summer in the southern United States favorinfection and development. The tissue is blighted, and webs of white myceliummay develop over the dead tissue under humid conditions. The sporangia (seen asblack specks) appear on the white mycelial webs (Fig. 17) and on cankered stems(Fig. 18). Poinsettias may show symptoms during propagation or soon after potting.In the northern Unites States, R. stolonifer causes a stem rot of poinsettia. A dark,greasy-looking discoloration extends 10 cm or more up from the stem base. Poin-settias may suddenly wilt and collapse; symptoms may be mistaken for bacterial softrot.

2.12.3 Biology and EpidemiologyR. stolonifer was reported as a pathogen of Euphorbia spp. previous to its docu-mentation as a pathogen of Gerbera jamesonii (African daisy), Crossandrainfundibuliformis (crossandra), Catharanthus roseus (annual vinca), and Sinningia

Fig. 17 Rhizopus blight

Fig. 18 Mycelium andsporulation of Rhizopusstolonifer on a canker


speciosa (gloxinia). It is particularly aggressive on E. milii (crown of thorns). Thefungus affects a wide range of non-ornamental hosts as well, most commonlycausing a soft rot of fruits. Annette Hegg poinsettia cultivars were reported to beless susceptible than V-14 Glory or V-14 White.

Spores of R. stolonifer are ubiquitous and survive desiccation. The pathogengrows rapidly at 21–32 �C/70–90 �F; disease develops only at a relative humidity ofmore than 75 %. R. stolonifer usually colonizes wounds as an opportunistic patho-gen, often affecting crops growing under stressful conditions.

2.12.4 ManagementPoinsettia crops should be maintained under optimal cultural conditions, becauseoutbreaks of this disease have generally followed periods of stress. It is particularlyimportant to maintain ideal conditions for prompt callusing and rooting of cuttings,since the cutting wound is a major point of entry for the fungus. Infected plant debrisshould be removed. No reports of effective fungicides have been made for Rhizopusblight on poinsettia.

2.13 Scab (Spot Anthracnose) (Sphaceloma poinsettiae Jenk.and Ruehle)

2.13.1 Geographic Occurrence and ImpactPoinsettia scab was initially reported on poinsettia from Florida (Ruehle 1941). Thedisease is distributed throughout subtropical and tropical America including Florida,Puerto Rico, and Hawaii, as well as the South Pacific, on the genus Euphorbia.During the late 1960s scab became less serious as disease-free cuttings becameincreasingly available. However, the rapid spread of scab-infected cuttings world-wide does happen occasionally.

2.13.2 Symptoms/SignsTan spots (1–4 mm in diameter) with 1- to 2-mm chlorotic haloes appear. The leaftissue may buckle, causing the leaves to distort somewhat (Fig. 19). Occasionally,larger necrotic areas may develop, with the entire leaf turning chlorotic and abscis-ing. Scab-like lesions can form on stems and petioles; these are 1–10 mm in diameterand may be either rounded or elongated. Lesions are usually tan and may have a redor purple margin. Stem lesions, which may be sunken and can contain fungal growth(Fig. 20) and gray sporulation (Fig. 21), may coalesce to girdle stems. One interest-ing characteristic is the abnormal growth of infected stems, which can be markedlylonger than uninfected stems on the same plant (Fig. 22).

2.13.3 Biology and EpidemiologyInoculation trials with isolates of S. poinsettiae from poinsettia showed thatE. heterophylla (Mexican fire plant), E. prunifolia (painted euphorbia), Manihotesculenta (cassava), and M. carthaginensis were all susceptible. Symptoms areapparent 7 days after stem inoculation, and younger leaves are more susceptible


than the older leaves. Conidia were produced 1 month after inoculation in one study;they are readily spread by splashing water from irrigation and rainfall.

Fig. 19 Leaf lesions ofpoinsettia scab (Sphacelomapoinsettiae)

Fig. 20 White lesions onstem due to scab (Sphacelomapoinsettiae)

Fig. 21 Stem lesions of scabbearing light brownsporulation


2.13.4 ManagementDisease-free cuttings should always be used: growers should make a thoroughexamination of all propagation material whether rooted or unrooted. A growershould not retain diseased stock plants from season to season. A trial in 2001 thatevaluated 42 cultivars showed that the cultivars with dark green leaves were slightlyless susceptible than cultivars with leaves having lighter green coloration (Daughtreyand Tobiasz 2002). Research at Cornell University and Michigan State Universityconcluded that all cultivars tested (in excess of 100 over a 4-year period) weresusceptible to Sphaceloma. The most sensitive cultivars included ChampagnePunch, Cranberry Punch, Strawberry Punch, Redberry Punch, Snowberry Punch,Freedom Fireworks, Freedom Pink, Freedom Coral, Jester Red, Peterstar White,Peterstar Pink, Peterstar Orange, Peterstar Marble, Winterfest Coral, Winterfest Red,Silver Star, Max Red, Eurostar, Chianti Red, Eternity Red, and Enduring Pink. Onthe other end of the spectrum, the lowest disease levels were seen on Classic Red,Holly Point, Jingle Bells, Strawberries and Cream, Thanksgiving Red, Winter RoseWhite, Winter Rose Pink, and Freedom Salmon.

Excellent prevention of scab with fungicides was found in one trial on FreedomRed with pyraclostrobin and boscalid (FRAC 7 and 11), azoxystrobin (FRAC 11),

Fig. 22 Hyper-elongatedstems are an indication of scabinfection


copper fungicides (FRAC M1), mancozeb (FRAC M3), and chlorothalonil (FRACM5) (Hausbeck et al. 2004b). In a 2000 trial on Freedom Red and Pink Success,good control with a 7-day interval was found with trifloxystrobin (FRAC 11), copperpentahydrate (FRAC M1), and triflumizole (FRAC 3). Reduction of symptoms withcombination products of copper hydroxide and mancozeb or thiophanate-methyl(FRAC 1) and chlorothalonil was also high, but residue after several weekly sprayswas excessive. Foliar residues from wettable powder products may be reduced byadding a spreader-sticker or wetting agent (Daughtrey and Tobiasz 2001).

2.14 Thielaviopsis Black Root Rot: Thielaviopsis basicola (Berk.and Broome) Ferraris (syn. Chalara elegans)

2.14.1 Geographic Occurrence and ImpactBlack root rot caused by Thielaviopsis basicola (syn. Chalara elegans) is foundworldwide, with the causal fungus affecting many hosts. This was a very commonand damaging disease in the early years of poinsettia production, but since the adventof growing poinsettias in soilless media, the incidence of the problem hasplummeted. Sanitation efforts by poinsettia propagators have also been creditedwith reducing this problem (Strider and Jones 1985).

Curiously, black root rot is today a severe and common problem in production ofcertain bedding plants, notably pansies and calibrachoas, grown in the same green-house operations as poinsettias that remain free from the disease. It is unclearwhether this is due to host specialization of the pathogen on the bedding plants orto reduced susceptibility of modern poinsettias.

2.14.2 Symptoms/SignsBlack root rot darkly discolors roots (Fig. 23), but generally leaves the tissues intact– in contrast to the more common Pythium root rot, which causes a lighter brown,softer rot. Another distinguishing trait is that Pythium root rot begins at the root tip,whereas T. basicola infection can occur anywhere on the root system (Perry 1971).Identification of the disease is best accomplished by direct examination of discoloredroot tissues under a compound microscope, as the pathogen grows slowly in standardlaboratory media and can be overlooked in the presence of faster growing microor-ganisms. The root system is diminished in size by early infections and will in allcases show sections that are darkened, in part by the brown chlamydospores(Fig. 24) of the fungus.

Affected plants are stunted if infection occurs before plant maturity, and foliagecan be undersized and chlorotic. In particular, the lower leaves of infected plants turnyellow, curl, and defoliate, similarly to leaves on plants with Pythium root rot. Leafspotting due to T. basicola was reported on one occasion (McCain and Raabe 1975).

The infection may be evident at the stem base, where dark brown chlamydospores(aleuriospores) accumulate on the stem en masse (Fig. 25). The stem may also showdark longitudinal cracks – a distinctive characteristic of black root rot (Bateman andDimock 1959).


Fig. 23 Dark brown rootdiscoloration results fromThielaviopsis basicola attackon poinsettias

Fig. 24 Darkchlamydospores of T. basicolain an infected root

Fig. 25 Black discolorationat the base of the stem is anindication of T. basicolaattack


2.14.3 Biology and EpidemiologyBlack root rot is generally thought of as a soilborne disease, but in greenhouses thereare opportunities for aerial or waterborne spread. The mycelium of T. basicolaproduces two kinds of spores, both of which are infectious. In addition to dark-walled chlamydospores, T. basicola forms hyaline phialospores, produced as endo-conidia, on the surface of the root. In the humid, still air of petri plates, theseendoconidia will develop as long chains of cylindrical spores on root lesionsincubated on moist filter paper. The phialospores may be airborne in greenhouses(Graham 1994), spreading the pathogen to noncontaminated growing media, buthow commonly this happens is not known. The phialospores are probably spreadthrough recirculating irrigation systems, but it was noted in 1994 that transmissionthrough a recirculating system had not been conclusively demonstrated (Stanghelliniand Rasmussen 1994), and no subsequent studies have been conducted to ourknowledge. The phialospores were initially thought to be short lived, but studieshave shown that they may persist in soil for months to over a year, depending uponfactors such as soil type (Schippers 1970).

The chlamydospores of T. basicola are generally produced in short chains of 1–8dark brown segments supported by 2–3 hyaline cells (Patrick et al. 1965) on rootsurfaces or within the root cortex. When fragmented into the individual spores, theyare more difficult to recognize. Fragmentation has been observed to be a necessaryprecursor to germination (Patrick et al. 1965). The chlamydospores are restingspores with the ability to survive years without a host (Stover 1959), so they presenta challenge for greenhouse sanitation.

Bateman (1961) established that high soil moisture is conducive to poinsettiainfection by T. basicola. The disease was very severe at 70 % moisture holdingcapacity and above. The infective phialospores can germinate quickly in wet soilseven without additional nutrients (Punja 1993). Chlamydospores also germinatereadily in wet soils (Linderman and Toussoun 1967).

Black root rot is encouraged by cooler soil temperatures. High temperaturesuppresses disease: in inoculated mineral soil, poinsettias showed severe root rot at13–26 �C/55–79 �F with a maximum at 17 �C/62 �F, but almost no symptoms at30 �C/86 �F or above (Bateman and Dimock 1959).

Soil pH has a strong effect on this disease: acidic soils are disease suppressive.Growing poinsettia at a pH of 4.8 prevented disease (Keller and Shanks 1955), andpH 5.5 or lower reduced the impact of black root rot or Pythium infection onpoinsettias grown in mineral soil (Bateman 1962).

Fungus gnats can disseminate the pathogen (Harris 1995). Shore flies have alsobeen shown to spread T. basicola chlamydospores aerially within a greenhouse(Stanghellini et al. 1999). See chapter “▶ Insect Management for Disease Controlin Florists’ Crops,” for additional information.

2.14.4 Management• Sanitation – Strider and Jones (1985) pointed out that black root rot was not as

important a disease in North Carolina as it had been in the past, and this was




attributed to the propagators’ efforts at improving sanitation during cuttingproduction, the use of soilless growing media, and preventive fungicide drenches.The disease is rarely seen today. Reuse of containers after black root rot outbreakswill lead to repeated occurrences of disease (Graham 1994). A hydrogen dioxidesanitizer at recommended rates and chlorine bleach (1:9 dilution of a 5.25 %solution) were shown to be highly effective disinfectants (Warfield 2003). Use ofbromine or quaternary ammonium compounds did not rid greenhouse surfaces ofT. basicola inoculum, whereas chlorine bleach at a 1:4 dilution (1.04 % sodiumhypochlorite) was effective on all surfaces tested (plastic, wood, and metal)(Copes and Hendrix 1996). Aerated steam heat treatment for 30 min at 50 �C/122 �F completely eliminated T. basicola from a soilless mix and was safe onplastic pots and trays (Linderman and Davis 2008).

• Cultural Control – Using a well-drained growing medium is important for blackroot rot avoidance. Avoiding a high pH that favors black root rot can be part of theoverall integrated pest management plan, but should not be used to the detrimentof the nutritional status of the plant. A pH low enough to suppress black root rot,pH 5.2 (Strider and Jones 1985), is lower than the recommended pH range forpoinsettia cultivation, pH 5.8–6.2 (Williams 2011).

• Biocontrol – Biocontrol of black root rot has not been developed for floricultureproduction systems. Fluorescent pseudomonads were identified (Stutz et al. 1986)in the microflora of soil suppressive to black root rot in tobacco, with their plant-protective effect being attributed in part to production of pathogen inhibitors suchas 2,4-diacetylphloroglucinol and/or hydrogen cyanide (Ramette et al. 2006). Amore recent study used microarrays to identify Azospirillum, Gluconacetobacter,Burkholderia, Comamonas, and Sphingomonadaceae associated with a soil sup-pressive to black root rot of tobacco (Kyselkova et al. 2009). A commercialformulation of Streptomyces griseoviridis reduced black root rot on citrus whenused at a high rate (0.03 %, 0.32 g/L) (Graham 1994).

• Fungicides – Benzimidazole fungicides (FRAC 1) were seen as the most effectiveagainst T. basicola in the past (Manning et al. 1970), and today one of thefungicides in this same mode of action group, thiophanate-methyl, has the bestreputation for management of the disease (Daughtrey 2006; Atwood 2013). Othermaterials should be used in rotation with thiophanate-methyl to fend off resis-tance development. Some of the effective choices would be the active ingredientspolyoxin D, triflumizole, and fludioxonil, found in fungicides in FRAC groups19, 3, and 12, respectively (Daughtrey et al. 2015). Fungicides may be used togood purpose to protect the remainder of the crop after a disease outbreak, butgreat effort should be expended at the end of the growing season to eliminate thefungus from the greenhouse.


3 Bacterial Diseases

3.1 Bacterial Canker [Curtobacterium flaccumfacienspv. poinsettiae (Starr and Pirone) Collins and Jones(Previously Corynebacterium flaccumfaciens subsp.poinsettiae)]

3.1.1 Geographic Occurrence and ImpactA bacterial blight of poinsettia was originally described from New Jersey in 1942(Starr and Pirone 1942). Widespread occurrence in old and new plants, homegardens, and nursery plantings as well as many separated localities indicated thatthe disease may have been present for many years prior to its initial identification(Creager 1959). It has been subsequently reported in Florida (McFadden andCreager 1960), Maryland, New York, Pennsylvania, Virginia (Salazar 1983), andNew Zealand. Disease outbreaks may result in extensive damage to the crop butappear to be rare.

3.1.2 Symptoms/SignsStems, leaves, and bracts may become blighted. In some cases, only branch cankersare noted, and disease incidence is often low in a particular crop. The bacteriumcauses elongated, water-soaked to brown streaks visible on the surface of the stem(Fig. 26). Irregular water-soaked to brown cankers that girdle the stem also can formand the stem tip may curve. Terminal leaves may become deformed; irregular brownspots develop and leaf abscission occurs. Severely cankered stems show longitudinalcracks and sometimes amber droplets containing bacteria are found (McFadden1959).

3.1.3 Biology and EpidemiologyEnvironmental sources of C. f. poinsettiae have not been identified. The bacteriumhas been recovered from asymptomatic, healthy-appearing, rooted poinsettia cut-tings; 10 % of asymptomatic plants tested were infected. The bacterium can ooze

Fig. 26 Bacterial cankercaused by Curtobacteriumflaccumfaciens pv. poinsettiae(Courtesy of Mary AnnHansen)


from infected leaves and stems and be splashed by irrigation water to adjacent plants.Infection of leaves occurs through stomates. It is probable that pruning tools andhands can transmit the bacterium from plant to plant during standard crop culture.Warm conditions and high nitrogen levels have been reported to be associated withdisease occurrence. Disease is not usually evident until the plants are close tofinishing.

3.1.4 ManagementPlants showing symptoms of this disease should be removed and discarded. Due tothe slow disease development, the location of the pathogen in the vascular system,and little if any plant-to-plant movement during the growing season, bactericidalsprays have not been evaluated and are not warranted. It is possible that bactericidesused for other bacterial pathogens are masking low levels of infection due to thebacterial blight pathogen.

3.2 Greasy Canker [Pseudomonas viridiflava (Burkholder)Dowson]

3.2.1 Geographic Occurrence and ImpactCanker on poinsettia caused by Pseudomonas viridiflava was described and namedgreasy canker in 1981 (Suslow and McCain 1981). The disease was also reported inFlorida (Engelhard and Jones 1990), and the pathogen has been cultured from stemsand foliage of diseased poinsettia in Massachusetts.

3.2.2 Symptoms/SignsThe first report of this disease described a canker and leaf spot as well as a bract andbud blight (Fig. 27). Cankers may originate at pruning wounds on the stem. Thecankered areas are greasy in appearance with no soft rot. They eventually turn lighttan to brown and, as the cuticle lifts from the stem, they take on a papery texture.Leaf spots are angular and randomly distributed.

3.2.3 Biology and EpidemiologyP. viridiflava, first described from green beans in 1927, is an opportunistic pathogen,reported to be an epiphyte on some plants and a secondary invader. Marginal leafnecrosis and necrotic spots on stems form on potted plant genera including Euphor-bia, Hibiscus, Capsicum, and Hydrangea. Inoculations of other hosts ofP. viridiflava from poinsettia strains were successful, showing no evidence of hostspecificity.

Inoculations of seven poinsettia cultivars showed no resistance to the bacterium.There are conflicting reports of the optimum temperature for disease development inpoinsettia. Suslow and McCain (1981) reported that severity was greater at27–32 �C/80–90 �F than at 25 �C/77 �F. However, tests in Florida indicated thatdisease was severe at 10 and 15 �C (50–59 �F), mild at 27.7 �C/82 �F, and absent at32.2 �C/90 �F. Because of this variability, it does not appear that temperature can be


used to predict disease occurrence or severity for P. viridiflava. No other studies ofgreasy canker on poinsettia have clarified this discrepancy of results, which mayhave been due to the cultivar of the host chosen and the specific strain ofP. viridiflava employed.

3.2.4 ManagementControl measures outlined for Xanthomonas leaf spot (below) are appropriate forgreasy canker. Plants known to be infected should be discarded and not used forpropagation. Although no bactericides have been demonstrated effective againstdiseases caused by P. viridiflava on poinsettia, it is likely that those effective onother bacterial diseases will have an impact.

3.3 Soft Rot and Stem Rot [Dickeya chrysanthemi (syn.Pectobacterium chrysanthemi) and Pectobacteriumcarotovorum (syn. Erwinia carotovora (Jones)) Holland.]

3.3.1 Geographic Occurrence and ImpactSoft rot on poinsettia cuttings was first reported from Missouri and attributed toErwinia carotovora by Rogers (1959); the pathogen was later renamedPectobacterium carotovorum. Another soft rot bacterium causing stem rot in poin-settia (Hoitink and Daft 1972), previously named Erwinia chrysanthemi orE. carotovora subsp. chrysanthemi, has now been moved to the genus Dickeya(Ma et al. 2007). Dickeya chrysanthemi was recently reported from China(Rungnapha et al. 2008).

Fig. 27 Poinsettia bractinoculated with Pseudomonasviridiflava


3.3.2 Symptoms/SignsOne of the most common symptoms on poinsettia is a cutting rot (Fig. 28). Duringpropagation, cuttings develop a water-soaked decay, beginning at the cutting wound.In other cases, symptoms may be delayed, so that extensive symptoms appearsuddenly in hot weather, presumably due to latent infections. Chlorotic spotsanywhere along the stem and purplish-black petioles are the first noticeable symp-toms. The spots rapidly coalesce, forming large, irregular, chlorotic areas. Petiolesturn black and shrivel and affected leaves wilt. Infected tissues are soft and watersoaked. Mature plants may also collapse from latent infections withD. chrysanthemiin hot weather.

3.3.3 ManagementMaintenance of proper shipping environment (temperature and moisture) minimizessubsequent development of soft rot on unrooted cuttings. Shading cuttings duringrooting is important for reducing stress, thus promoting fast rooting and reducingbacterial cutting rot. A waterlogged growing medium is conducive to diseasedevelopment. Growers report that water management during propagation is thekey to preventing cutting rot due to soft rot bacteria. Typically, no bactericides areused.

3.4 Xanthomonas Leaf Spot [X. axonopodis pv. poinsettiicola(Patel et al. 1951) Vauterin, Hoste, Kersters, and Swings 1995(syn. X. campestris pv. poinsettiicola)]

3.4.1 Geographic Occurrence and ImpactLeaf spot of poinsettia caused by a Xanthomonas species was first observed in Indiain 1951 (Patel 1951). The disease was later described in Florida in 1962, and in 1985a xanthomonad was reported on Codiaeum (croton – another euphorbiaceous plant)that was able to infect both croton and poinsettia. The pathogen previously namedXanthomonas campestris pv. poinsettiicola was separated into three species in 1995

Fig. 28 Bacterial soft rot inpropagation


on the basis of DNA:DNA homology, with the pathogen most often associated withpoinsettia separated out as X. axonopodis pv. poinsettiicola. Classification of thesebacteria is not yet entirely resolved. Two other pathovars of X. campestris have alsobeen reported to cause leaf spot on poinsettia: X. c. euphorbiae (Sabet, Ishag, andKhalil) Dye and X. c. manihotis (Berthet and Bondar) Dye have been reported tocause poinsettia leaf spot upon inoculation. Although Xanthomonas leaf spotappeared rarely in poinsettia production in the past, in the late 1990s and continuingtoday, it is found in many locations worldwide: Slovenia (Dreo et al. 2011), Norway(Perminow et al. 2011), China (Li et al 2006), Austria (Gottsberger and Plenk 2009),Taiwan (Lee et al. 2006), and Italy (Stravato et al. 2004).

3.4.2 Symptoms/SignsSpots are at first visible on the undersurface of the leaf as gray to brown, water-soaked lesions (Fig. 29). As they enlarge to 2–3 mm, they become visible on the topsurface of the leaf and are chocolate brown to rust colored and may or may not havepale green halos. Spots may coalesce into large areas of blighted tissue. Severelyspotted leaves turn yellow and abscise.

3.4.3 Biology and EpidemiologyIn a Florida inoculation trial, X. campestris pv. poinsettiicola was shown to bepathogenic to poinsettia and to croton, Codiaeum variegatum (L.) Blume (Chase1985). The latest taxonomic revision separates out the bacteria pathogenic toCodiaeum as X. codiaei and uses the name X. axonopodis pv. poinsettiicola for thepoinsettia pathogen, but there is likely some overlap in their host ranges. X. c.euphorbiae causes leaf spot on E. acalyphoides (a weed from Sudan) and will spotpoinsettia upon inoculation. X. c. manihotis is a non-pigmented xanthomonad and ispathogenic to Manihot esculenta Crantz (cassava) and to poinsettia upon inocula-tion. Recently, a study of xanthomonads associated with poinsettia leaf spot over a64-year period has uncovered additional genetic diversity in the bacteria able tocause symptoms on poinsettia (Rockey et al. 2015); now we ascribe what we havelong considered one bacterial leaf spot disease of euphorbs to multiple pathogens

Fig. 29 Xanthomonas leafspot (Xanthomonasaxonopodis pv. poinsettiicola)


within the genus Xanthomonas and anticipate further clarification with additionalresearch.

Little has been published on the epidemiology of bacterial leaf spot on poinsettia,but it has been reported to spread rapidly, presumably from splashing water and fromworker handling. If epiphytic populations occur, as is known with other diseasescaused by xanthomonads, then colonized, asymptomatic cuttings may developdisease under favorable conditions.

3.4.4 ManagementAffected plants should be discarded, and no cuttings should be taken from plantswith leaf spots. Wetting of foliage should be avoided, especially during periods thatwould extend the leaf wetness duration.

Some work has been conducted to identify potential leaf-associated bacterialstrains for biological control of the pathogen (Li et al. 2008) from China. Twostrains with promise were identified as Bacillus amyloliquefaciens (PAB241 andPAB242).

Poinsettia plants treated with titanium dioxide (TiO2 at 25 and 75 mM) showed85–87 % and 92–93 % reductions in lesions, respectively. No phytotoxicity wasobserved (Norman and Chen 2011). Studies with conventional products have beengenerally less successful. In one trial acibenzolar drench and mancozeb (FRAC M3)provided the best control, followed by acibenzolar foliar spray (which was moder-ately phytotoxic) and cupric hydroxide (FRAC M1). In another trial, copper penta-hydrate (FRAC M1) and didecyl dimethyl ammonium chloride (DDAC) (FRACNC) provided excellent prevention.

3.5 Poinsettia Branch-Inducing Phytoplasma (CandidatusPhytoplasma sp.)

Phytoplasmas are plant pathogenic bacteria in the class Mollicutes that are restrictedto phloem, resulting in symptoms that include yellowing, stunting, flower malfor-mation, and witches’ brooms (Lee et al. 2000; Chaturvedi et al. 2010). Although adisease, infection of poinsettias with the poinsettia branch-inducing phytoplasma(PoiBI) introduces welcome rather than undesirable traits because it promotesbranching to give the potted poinsettia a fuller and more compact form.

3.5.1 Geographic Occurrence and ImpactThis phytoplasma affects poinsettias all over the world. Chen et al. (2007) examinedmultiple poinsettia cultivars originating from the United States and Europe andfound all of them to carry phytoplasmas.

3.5.2 Symptoms/SignsPoinsettias infected with this phytoplasma have less apical dominance and showmore growth from axillary branches than those lacking the pathogen (Fig. 30). Someside effects of the phytoplasma infection include shorter internodes, shallower leaf


lobes, thinner stems, paler bract color, earlier anthesis, and cyathia abortion andlower fertility (Preil 1994).

3.5.3 Biology and EpidemiologyThe main poinsettia phytoplasma belongs to 16SrIII-H, a subgroup of the X-diseasegroup (Chaturvedi et al. 2010). However, there are three additional types of phyto-plasma that have been found in poinsettia (Pondrelli et al. 2002): the B and Csubgroups of 16Sr1 and 16SrXII-A are also sometimes found by PCR. The 1967cultivar ‘Annette Hegg’ was the first to show the desirable trait of free branching. Itwas discovered that the trait was graft transmissible (Stimart 1983). Many attemptswere made to identify the branching factor. In 1997 a phytoplasma was determinedto be the branch-inducing factor (Lee et al. 1997), and it was shown that there weremultiple phytoplasmas occurring in poinsettia (Abad et al. 1997). PCR tests may beused to identify the presence of phytoplasmas in poinsettia. A comparison of geneexpression in infected vs. healthy poinsettia (Nicolaisen and Christensen 2007)indicated increased expression of cytokinin biosynthesis genes in plants containingphytoplasma.

3.5.4 ManagementTetracycline has been used to cause reversion of poinsettia from the free-branchingform to the healthy form (Bradel et al. 2000a). Since the diseased form is moredesirable in the trade, however, the tetracycline treatment is primarily useful forresearch purposes.

Fig. 30 The plant at leftexhibits the morphologyinduced by the poinsettiabranch-inducingphytoplasma, in contrast to aphytoplasma-free plant of thesame cultivar at right(Courtesy of MichaelKlopmeyer)


4 Viruses

4.1 Poinsettia Mosaic (Poinsettia mosaic virus PnMV)

4.1.1 Geographic Occurrence and ImpactThis virus is likely to be found in commercially grown poinsettias all over the worldand also affects Euphorbia fulgens (Koenig et al. 1986). In a survey in BritishColumbia (Chiko 1983) in 1981, PnMV was found in eight of nine cultivars tested(all Annette Hegg types) and in 94 % of the 65 samples.

4.1.2 Symptoms/SignsPoinsettias with PnMV may show malformed leaves or bracts and a systemic mosaicof the foliage (Fig. 31) (Fulton and Fulton 1980). Expression of symptoms is thoughtto be greater at cooler temperatures (Fulton et al. 1978); symptoms were noted inwinter but not in summer in Queensland, Australia (Gordon et al. 1996).

4.1.3 Biology and EpidemiologyParticles of PnMVare icosahedrons 26–29 nm in diameter. Although when initiallycharacterized PnMV was thought to be a tymovirus (Fulton and Fulton 1980),studies on PnMV recently provided good evidence that the virus is instead aMarafivirus, and it has now been designated a species of the genus Marafivirus(Bradel et al. 2000b; Koenig et al. 1986). PnMV was transmitted by grafting to twoother euphorbias: E. cornastra (Dressler) A. Radcliffe-Smith, which was symptom-less, and E. bubalina Boiss., which showed a mild mosaic (Fløistad and Blystad1999). There is no evidence of seed transmission; the virus is transmitted by

Fig. 31 Mosaic caused byPoinsettia mosaic virus(Courtesy of Dag-RagnarBlystad)


mechanical inoculation. Curiously, although no vector is known, plants freed fromPnMV have been seen to become reinfected quickly (Blystad and Fløistad 2002).

Standard production practices did not allow disease spread in one trial(Pfannenstiel et al. 1982), yet commercial propagators have had difficulty riddingtheir poinsettias of the virus. Pfannenstiel et al. (1982) were able to cure shoots of theviral infection with heat therapy (32 �C/90 �F for at least 9 weeks), and then to graftthese shoots to disease-free rootstocks, so it seems that clean stock should beobtainable.

4.1.4 ManagementEfforts by Bech and Rasmussen (1996) were effective at curing poinsettias of PnMV.They used meristem-tip culture to eliminate PnMV from ‘Freedom’ poinsettia, butthe branching of the resulting plant indicated Freedom from the poinsettiabranching-inducing phytoplasma as well and thus was unacceptable. A temperaturetreatment of ‘Lilo’ resulted in plants free from PnMV but branching normally. UsingRNA silencing methodology, transgenic poinsettias were developed that were resis-tant to mechanical inoculation of PnMV (Clarke et al. 2008).

4.2 Poinsettia Latent Virus (PnLV)

Poinsettia latent virus (PnLV) causes no symptoms in poinsettia and was earliernamed poinsettia cryptic virus (Koenig and Lesemann 1980). It has icosahedralparticles and is a chimera, with genetic features of both poleroviruses andsobemoviruses (Aus dem Siepen et al. 2005). It is found in many commercial linesof poinsettia today, where it occurs along with poinsettia mosaic virus (PnMV) andthe phytoplasma that causes free branching.

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Documents

Diseases of Poinsettia … · a wealth of foliar problems (Botrytis blight, powdery mildew, scab, Alternaria leaf spot, Xanthomonas leaf spot, andanthracnose) as well as many commonroot