Spraying Leaves of Pear Nursery Trees withUrea and Copper EthylenediaminetetraaceticAcid Alters Tree Nitrogen Concentrationwithout Influencing Tree Susceptibility toPhytophthora syringae

S. Laywisadkul1,3, C.F. Scagel2, L.H. Fuchigami1, and

R.G. Linderman2

ADDITIONAL INDEX WORDS. defoliant, fertilizer, phosphonate, Pyrus communis

SUMMARY. Recent field observations by growers suggest that increased nitrogen (N)content in nursery trees resulting from foliar sprays with urea in the autumnincreases tree susceptibility to infection by Phytophthora syringae. We investigatedthe effects of soil N availability and spraying pear (Pyrus communis ‘OHF 97’) treeswith combinations of urea, chelated copper ethylenediaminetetraacetic acid(CuEDTA), and phosphonate-containing fungicides on stem N concentration andsusceptibility to infection by P. syringae. Increasing soil N availability increasedsusceptibility to P. syringae and increased N and amino acid concentration in stems.Spraying trees with urea in the autumn increased concentrations of N and aminoacids in stems and had no significant effect on tree susceptibility when stems wereinoculated with P. syringae before or after urea sprays. Spraying trees with CuEDTAdecreased stem N concentrations and had no significant influence on tree suscep-tibility to P. syringae when stems were inoculated before or after CuEDTA sprays.These results suggest the relationship between tree susceptibility to P. syringae andtree N concentration may be specific to the form of N, delivery method, or timing ofN applications. Trees had higher N concentrations in stems in November than inOctober and were more susceptible to P. syringae when inoculated in November,suggesting that environmental factors and increasing tree dormancy may beresponsible for changes in susceptibility to the pathogen. Spraying trees withfungicides containing fosetyl-aluminum in October or November decreased treesusceptibility to P. syringae. The effects of fungicides containing fosetyl-aluminumon susceptibility were similar regardless of whether trees were sprayed or not withurea or CuEDTA, suggesting that these fungicides can be used in combination withurea or CuEDTA sprays for reducing disease severity caused by P. syringae withoutimpacting growers’ objective of increasing tree N content with urea or enhancingearly defoliation with CuEDTA.

Diseases caused by species ofPhytophthora are responsiblefor significant economic losses

on a wide range of host plants, in-cluding pear (Erwin and Ribeiro,1996; Harris, 1979; Wormald, 1919).Disease caused by Phytophthora syringaeoccurs during the winter in nurserystock in the Pacific northwest region

of the United States (PNW), especiallyon trees that are harvested and storedin coolers or in outdoor sawdust beds(Erwin and Ribeiro, 1996; Pscheidt andOcamb, 2002; Tidball and Linderman,1990). The fungus spreads via splashdispersal of inoculum from soil toleaves, stems, and fruit (Ristaino andGumpertz, 2000; Upstone, 1978), and

infects trees through wounds on stemscaused by handling or pruning orthrough leaves and leaf scars (Bostockand Doster, 1985; De Bruyn, 1924).In nursery stock, dark, sunken cankersoccur on stems, and in severe cases, thestem is girdled (Erwin and Ribeiro,1996; Young and Milbrath, 1959).

Most pear varieties in the PNWare grafted on selected rootstock clon-ally propagated in nurseries and de-foliated before harvesting and coldstorage, similar to production practicesused for many other deciduous nurserytrees (Frecon, 1982). Methods usedfor defoliation include manual or me-chanical removal of leaves and theuse of chemical sprays [e.g., chelatedcopper ethylenediaminetetraacetic acid(CuEDTA)] that result in early abscis-sion of leaves, usually while the leavesare still green. Chemical-induced de-foliation of deciduous trees decreasesthe amount of N mobilized from leavesto stems and roots in the autumn; thus,it can reduce N reserves required forgrowth the following spring (Bi et al.,2003; Guak et al., 2001). The combi-nation of foliar sprays with urea andCuEDTA can be used to obtain effi-cient early defoliation and promoteN storage without reducing plantgrowth performance the followingyear (Bi et al., 2005; Guak et al.,2001). Early defoliation before termi-nal buds set can also inhibit the de-velopment of dormancy and coldhardiness (Fuchigami, 1970). To sur-vive in cold storage and grow wellduring the following growing season,trees must have enough reserve nutri-ents and develop dormancy.

Surface wounds inflicted duringharvest and leaf scars caused by artificialor natural defoliation and subsequenthandling can serve as infection open-ings for P. syringae, but the pathogen isunsuccessful in causing infection ofuninjured bark (Bostock and Doster,1985; De Bruyn, 1924; Linderman,

UnitsTo convert U.S. to SI,multiply by U.S. unit SI unit

To convert SI to U.S.,multiply by

29.5735 fl oz mL 0.03383.7854 gal L 0.26422.54 inch(es) cm 0.3937

25.4 inch(es) mm 0.03940.001 ppm g�L–1 10000.001 ppm mg�g–1 10001 ppm mg�L–1 10.001 ppm mL�L–1 1000

(�F – 32) O 1.8 �F �C (1.8 · �C) + 32

This work was funded in part by the U.S. Departmentof Agriculture-Agricultural Research Service, North-west Center for Nursery Crop Research

Mention of a trademark, proprietary product, orvendor does not constitute a guarantee or warrantyof the product by the U.S. Department of Agricultureand does not imply its approval to the exclusion ofother products or vendors that also may be suitable.

1Department of Horticulture, Oregon State Univer-sity, Corvallis, OR 97331

2U.S. Department of Agriculture, Agricultural Re-search Service, Horticultural Crops Research Unit,3420 NW Orchard Avenue, Corvallis, OR 97330

3Corresponding author. E-mail: srisangwan@gmail.com.

• April 2010 20(2) 331

1986; Pscheidt and Ocamb, 2002).Recently, growers of pear nursery treesin the PNW have reported increasedincidence and severity of damage totrees by P. syringae when ‘Old Home ·Farmington 97’ pear (‘OHF 97’) root-stock is sprayed with urea and chemicaldefoliants. It was hypothesized thatthe combination of urea and defolianttreatment predisposes the trees toP. syringae infection by inflicting injuryto the stem tissue or by indirectly mak-ing the trees more susceptible to in-fection by increasing tree N content.With other plant pathogens, abundantN can make trees more susceptibleto pathogens and increase the lengthof time trees are more susceptible(Frecon, 1982; Simon et al., 2003).

Infection of bare-rooted nurserytrees by P. syringae during cold stor-age could result from subjecting treesto environmental conditions that fa-vor the growth of the pathogen and/or are unfavorable to maintaining op-timal physiological condition of theplant (Pscheidt and Ocamb, 2002).The combination of host predisposi-tion and cold, wet conditions in coldstorage or outdoors favorable for path-ogen activity increases the potentialfor disease. In addition, P. syringae in-fection might be favored by the phys-iological or physical condition of theplant during harvesting and subse-quent handling and storage. It is pos-sible that trees harvested before theyare dormant may be more susceptibleto P. syringae and that surface woundsor leaf scars resulting from urea anddefoliant sprays and harvesting andhandling procedures could also serveas infection openings for P. syringae.

Increased damage by P. syringaehas not been reported for the majorityof plant species that are sprayed withurea and defoliants during produc-tion. Some nurserymen report thatearly defoliation of trees treated withthe combination of urea and defoliantmay actually reduce the incidence orseverity of diseases (L. Lyon, personnelcommunication). Reduced disease in-cidence and severity in response toearly defoliation may be a result ofmore complete healing of leaf scarsbefore the cold, wet conditions inthe autumn when the potential forP. syringae infection is high. Addition-ally, early defoliation enables trees tobe harvested and stored before the on-set of environmental conditions thatpromote the activity and subsequent

infection by P. syringae (Bostock andDoster, 1985). The effect of urea anddefoliants on disease incidence andseverity caused by P. syringae appearsto be species specific and may be re-lated to the time autumn sprays areused during production.

Common control measures forP. syringae in nursery production in-clude a combination of good nurserysanitation practices and chemical appli-cation. Phosphonate-containing fun-gicides, including fosetyl-aluminum(fosetyl-Al) and its breakdown prod-uct, phosphorous acid (also referredto as phosphonate) are commonlyused to control Phytophthora species(Doster and Bostock, 1988; Erwin andRibeiro, 1996). It is applied to trees assprays, drenches, dips, or by injection(Erwin and Ribeiro, 1996; Pegget al., 1987; Quimete and Coffey,1989; Tidball and Linderman, 1990).Fosetyl-Al translocates upward anddownward (in the transpiration streamand in the phloem sap) and may havedirect fungal toxicity activity againstPhytophthora species, or induces hostplant resistance (Erwin and Ribeiro,1996). Although chemical controlmeasures exist for this pathogen, theinfluence of these chemicals on con-trolling the disease may be affectedby the use of urea and defoliant spraysduring nursery production.

Our specific objectives were todetermine whether susceptibility offield-grown pear trees to P. syringaeis related to N concentration in stemsand is altered by spraying trees withurea or the defoliant CuEDTA at dif-ferent times in the autumn beforeand after inoculation with the patho-gen. Additionally, we also evaluatedwhether the effects of fungicides con-taining fosetyl-Al and phosphorousacid on P. syringae are altered byspraying trees with urea or CuEDTA.

Materials and methodsINOCULUM PRODUCTION AND

WOUND INOCULATION. Stock culturesof P. syringae [isolated from moun-tain laurel (Kalmia latifolia) by R.Linderman, USDA-ARS, Corvallis,OR] were maintained on V8 juiceagar (V8A) medium (Guo and Ko,1993) in the dark at 20 �C. Freshcultures were prepared 7 to 10 dbefore inoculation by transferring4-mm-diameter agar plugs to platescontaining V8A medium and incu-bated in the dark at 20 �C. Wounds

on stems were inoculated using myce-lial plugs (4 mm diameter) taken fromthe actively growing margin of coloniesof P. syringae growing on V8A me-dium. Plugs with or without the path-ogen were placed into a wound madewith a cork borer (4 mm diameter).Three wounds were made on the stemof each tree and two wounds wereinoculated with plugs of P. syringaegrown on V8A and one wound wasinoculated with plugs of V8A.Woundswere wrapped with wax-coated plasticfilm (parafilm� M; Alcan, Montreal,QC, Canada) after inoculation.

EXPERIMENT 1. Nursery-grownpear ‘OHF 97’ rootstocks wereplanted into1-gal containers filledwitha mixture ofdouglas firbark, peatmoss,and pumice (1:1:1 by volume) on 26Mar. 2002. The trees were grown ina lathhouse atOregonState University(OSU), Corvallis (lat. 44�30’N, long.123�17’W), trained to a single stem,and fertigated with 400 mL of acomplete fertilizer containing 20N–8.8P–16.6K (150 mg�L–1 Plantex�20–20–20 with micronutrients; Plan-tex, Brampton, ON, Canada) onceper week from 18 June to 30 July2002.

In Aug. 2002, 144 trees wereselected for uniformity based on stemdiameter (7–8 mm) and divided intothree groups of 48 trees. Trees ineach group were fertigated twice perweek (N fertigation treatment) with400 mL of modified Hoagland’ssolution number 2 (Hoagland andArnon, 1950) containing 0, 100, or200 mg�L–1 total N from ammoniumnitrate (NH4NO3). Trees in each fer-tigation treatment were divided intofour groups of 12 trees and leaves ontrees in each group were sprayed un-til runoff (autumn spray treatments)with 1) water on 26 Oct. 2002 and 9Nov. 2002, 2) urea (30 mL�L–1 urea,46N–0P–0K) on 26 Oct. 2002 andwater on 9 Nov. 2002, 3) water on 26Oct. 2002 and CuEDTA (10 mL�L–1

Librel�; Ciba, Suffolk, VA) on 9 Nov.2002, or 4) urea on 26 Oct. 2002 andCuEDTA on 9 Nov. 2002. Stemson six trees in each N fertigation ·autumn spray treatment combinationwere inoculated with the pathogen 7 dbefore sprays (19 Oct. 2002) or 7 dafter sprays (16 Nov. 2002). Inoculumproduction and wound inoculation wasperformed as described above.

Disease severity (length of lesionin centimeters) was measured on trees

332 • April 2010 20(2)

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after natural defoliation occurred ontrees sprayed with water (21 Dec.2002). Stems were removed fromtrees using pruning shears and wereplaced into a –80 �C freezer, freeze-dried, then ground with a Wiley mill(20 mesh) and regroundwith a cyclonemill (60 mesh). The N concentrationof ground samples was determinedusing the Kjeldahl method (Hornecket al., 1989). Concentrations of freeamino acids were determined by theninhydrin assay (Yemm and Cocking,1955).

The experiment was a completelyrandomized design with three factors:N fertigation rate in August (0, 100,and 200 mg�L–1 N), autumn spraytreatment (water, urea, CuEDTA,and urea + CuEDTA), and inoculationtime (before or after autumn spraytreatments). Each treatment had sixreplications. No lesions occurred onwounds inoculated with only V8A;therefore, only lesion size data fromwounds inoculated with the pathogenwere included in the analyses. Datawere analyzed using multivariate anal-ysis of variance (MANOVA) in a com-plete factorial design to determinewhether treatments influenced N andamino acid concentrations in stems,and lesion size on stems. MANOVAwas used to control experiment-wideerror rate before further univariateanalysis. When the overall multivariatetest was significant for a main effect orinteraction, the univariate F-tests foreach variable was examined to identifythe specific dependent variables thatcontributed to the significant overalleffect. Means for significant main ef-fects or their highest order interactionsfrom MANOVA are presented in fig-ures and were separated using Tukey’shonestly significant difference at P <0.05 (THSD0.05). Polynomial contrastswere used to evaluate the influence ofN fertigation rate on response vari-ables. Relationships between lesion sizeand stem N and amino acid concentra-tions were assessed using Pearson’scorrelation coefficient (r). Binomialanalyses (Wald Statistic, W) were usedto determine treatment effects on dis-ease incidence and data from significant(P < 0.05) factor interactions are pre-sented in figures. All statistical analyseswere performed with S-Plus (version6.0; MathSoft, Seattle) and Statistica(version 8.0; Statsoft, Tulsa, OK).

EXPERIMENT 2. Pear ‘OHF 97’rootstocks were planted into 1-gal

containers filled with a mixture ofdouglas-fir bark, peatmoss, and pum-ice (1:1:1, by volume) on 21 May2003. The trees were grown in a lathhouse at OSU, trained to a singlestem, and fertigated with a completefertilizer with micronutrients (200mg�L–1 Plantex� 20–20–20 with mi-cronutrients) once per week from 6June to 5 Sept. 2003.

In Oct. 2003, 80 trees wereselected for uniformity based on stemdiameter (7–8 mm) and divided intotwo groups of 40 trees. Trees in eachgroup were sprayed with a factorialcombination of urea, defoliant, andfungicide treatments on 5 Oct. 2004or 13 Nov. 2004. At each spray date,leaves on five trees were sprayed untilrunoff with one of a factorial combi-nation of urea treatment (water or30 mL�L–1 urea), defoliant treatment(water or 10 mL�L–1 CuEDTA), andfungicide treatment [water or a fungi-cide solution composed of fosetyl-Aland silica (6 g�L–1 Alliette�; BayerCrop Science, Research TrianglePark, NC)]. Stems on five trees ineach treatment combination were in-oculated with P. syringae 1 week afterspray treatments (12 Oct. 2003and 20 Nov. 2003). Inoculum pro-duction, wound inoculation, andassessment of disease severity wereperformed as described above.

Length of lesions (cm) was mea-sured on trees 8 weeks after inocula-tion. Stems of trees inoculated on 12Oct. 2003 and 20 Nov. 2003 wereassessed on 7 Dec. 2003 and 15 Jan.2004, respectively. After each assess-ment, stems were removed from treesusing pruning shears, and N concen-tration of stems was determined asdescribed above.

The experiment was a completelyrandomized design with four factors:Time of spray treatment (October orNovember), urea treatment (wateror urea), defoliant treatment (wateror CuEDTA), and fungicide treat-ment (water or fosetyl-Al). Each treat-ment had five replications. No lesionsoccurred on wounds inoculated withonly V8A. All stems inoculated withthe pathogen developed lesions ex-cept stems from treatments that in-cluded fosetyl-Al (data not shown).Only one stem from a tree sprayedwith fosetyl-Al developed lesions;therefore, only lesion size data fromstems not sprayed with fosetyl-Alwere included in statistical analyses.

All data were tested for homogeneityof variance using Levene’s test and fornormality using the Kolmogorov-Smirnov test. Lesion size data fromtreatments not including fosetyl-Alcould not be transformed to meethomogeneity of variance assumptionsof analysis of variance (ANOVA);therefore, data were analyzed usingKruskal-Wallis ANOVA at P < 0.05(K-W0.05) by comparing specific treat-ment combinations. Lesion size datawere assessed using K-W0.05 acrossspray treatments (water, urea,CuEDTA, and urea + CuEDTA) andspray time (October and November)to compare spray treatment effects onlesion size at different spray times(spray treatment · spray time interac-tion). N concentration data from allstems were analyzed in a completefactorial design with spray time, ureatreatment, and defoliant treatmentas main effects using ANOVA to de-termine whether treatments influencedstem N concentration. Means for sig-nificant main effects or their highestorder interactions from ANOVA arepresented in figures and were separatedusing THSD0.05. The relationships be-tween lesion size and stem N concen-tration were assessed using Spearman’srank correlation (R).

EXPERIMENT 3. Pear ‘OHF 97’rootstocks were planted into 1-galcontainers filled with a mixture ofdouglas-fir bark, peatmoss, and pum-ice (1:1:1 by volume) on 1 June 2004.The trees were grown in a lath houseat OSU, trained to a single stem, andfertigated with a complete fertilizerwith micronutrients [200 mg�L–1 Plan-tex� 20–20–20 with micronutrients]once per week from 14 June to 18Aug. 2004.

In Oct. 2004, 128 trees wereselected for uniformity based on di-ameter (9 mm) and divided into twogroups of 64 trees. Trees in eachgroup were sprayed with a factorialcombination of urea and fungicidetreatments on 22 Oct. 2004 or 24Nov. 2004. At each spray date, leaveson 16 trees were sprayed until runoffwith one of a factorial combination ofurea treatment (water or 30 mL�L–1

urea and 10 mL�L–1 CuETDA), andfungicide treatment {water or a fungi-cide solution composed of phospho-rous acid (H3PO3) neutralized withpotassium hydroxide (KOH) [PFOS(10 mL�L–1 PhytoFos�; Sipcam AgroUSA, Research Triangle Park, NC)]}.

• April 2010 20(2) 333

Stems on four trees in each treatmentwere inoculated with P. syringae 1week before spray treatments [–7 d(15 Oct. 2004 or 17 Nov. 2004)], or2 d [2 d (24 Oct. 2004 or 26 Nov.2004)], 1 week [7 d (29 Oct. 2004or 1 Dec. 2005)], or 3 weeks [21 d(12 Nov. 2004 or 15 Dec. 2004)]after spray treatments). Inoculumproduction, wound inoculation, andassessment of disease severity wereperformed as described above. Addi-tionally, three inoculations were alsomade on the same stem of eachtree without artificially wounding thestem: two locations were inoculatedwith the pathogen grown on V8A andone location was inoculated with V8A.

The length of lesions was mea-sured on trees 8 weeks after inocula-tion. Stems of trees inoculated at –7,2, 7, and 21 d in the October spraytreatments were assessed on 10 Dec.2004, 19 Dec. 2004, 24 Dec. 2004,and 7 Jan. 2005, respectively. Stemsof trees inoculated at –7, 2, 7, and 21d in the November spray treatmentwere assessed on 12 Jan. 2005, 21Jan. 2005, 26 Jan. 2005, and 9 Feb.2005, respectively. All stems wereharvested using pruning shears, andN concentration of stems was deter-mined as described above.

The experiment was a completelyrandomized design with four factors:Time of spray application (October orNovember), urea treatment (water orurea + CuEDTA), fungicide treat-ment (water or PFOS), and time ofinoculation (–7, 2, 7, or 21 d). Eachtreatment had four replications. Nolesions occurred on wounds inocu-lated with only V8A and no lesionsoccurred on stems inoculated with-out wounds; therefore, only lesionsize data from wounds and stemsinoculated with the pathogen wereincluded in the analyses. All data weretested for homogeneity of varianceusing Levene’s test and for normalityusing the Kolmogorov-Smirnov test.Lesion size data could not be trans-formed to meet homogeneity ofvariance assumptions of ANOVA;therefore, data were analyzed usingKruskal-Wallis ANOVA by compar-ing specific treatment combinations.Lesion size data were assessed usingK-W0.05 across spray treatment (wa-ter, urea, PFOS, and urea + PFOS)and spray times (October and No-vember) to compare spray treatmenteffects on lesion size at different spray

times (spray treatment · spray timeinteraction); across spray time and in-oculation times (–7, 2, 7, and 21 d) todetermine whether timing of patho-gen presence influenced lesion sizeat different spray times (inoculationtime · spray time interaction); andacross spray treatments and inocula-tion times to determine whether tim-ing of pathogen presence influencedlesion size of trees spray with differenttreatments (spray treatment · inocu-lation time interaction). N concentra-tion data from all stems were analyzedin a complete factorial design withspray time, urea treatment, fungicidetreatment, and inoculation time asmain effects using ANOVA to deter-mine whether treatments influencedstem N concentration. Means forsignificant main effects or their high-est order interactions from ANOVAare presented in figures and were sep-arated using THSD0.05. The relation-ships between lesion size and stem Nconcentration were assessed using R.

ResultsEXPERIMENT 1. All stems inocu-

lated with P. syringae 7 d after beingsprayed developed lesions, and inoc-ulating trees after spraying resulted insimilar or higher disease incidencethan inoculating trees before spraying(Fig. 1, A and E). Stems from treesinoculated after spraying had similaror lower N and amino acid concen-trations and developed larger lesionsthan stems from trees inoculated be-fore spraying (Fig. 1, B–D and F–H).There were positive correlations be-tween lesion size and stem N (R =0.660; P < 0.05) and amino acid (R =0.503; P < 0.05) concentrationswhen stems were inoculated beforebeing sprayed and positive correla-tions between lesion size and stem N(R = 0.597; P < 0.05) and amino acid(R = 0.494; P < 0.05) concentrationsafter being sprayed.

Stems from trees sprayed withwater or CuEDTA alone had similardisease incidence and lesion size andlower N and amino acid concentra-tions than stems from trees sprayedwith urea or a combination of ureaand CuEDTA (Fig. 1, E–H). Therewere positive correlations betweenlesion size and stem N (R = 0.578;P < 0.05) and amino acid (R = 0.505;P < 0.05) concentrations when treeswere sprayed with urea and positivecorrelations between lesion size and

stem N (R = 0.543; P < 0.05) andamino acid (R = 0.507; P < 0.05)when trees were sprayed with a com-bination of urea and CuEDTA. Therewere no correlations between lesionsize and stem N and amino acid con-centrations when trees were sprayedwith water or CuEDTA alone (R <0.163; P > 0.05).

Increasing N rate in August in-creased stem N and amino acid con-centrations and the size of lesions onstems from trees in all spray treat-ments (Fig. 1, J–L). On average,stems from trees grown with no Nduring August had similar or lowerdisease incidence, smaller lesions, andlower N and amino acid concentra-tions than stems from trees grownwith 100 or 200 mg�g–1 N duringAugust (Fig. 1, A–D). The influenceof August N rate on stem N concen-trations was greater when trees weresprayed with urea or a combination ofurea and CuEDTA than when treeswere sprayed with water or CuEDTAalone (Fig. 1K). The influence ofAugust N rate on lesion size and stemamino acid concentration was greaterwhen trees were sprayed with urea,CuEDTA, or a combination of ureaand CuEDTA than when trees weresprayed with water (Fig. 1, J and L).

EXPERIMENT 2. Lesions devel-oped on over 100% of wounds in-oculated with the pathogen except onstems from treatments that includedfosetyl-Al (data not shown). Stemsfrom trees sprayed in October devel-oped smaller lesions and had similaror higher N concentrations thanstems from trees sprayed in Novem-ber (Fig. 2, A and B). Stems fromtrees sprayed with water in Octoberhad lower N concentrations and de-veloped larger lesions than stemsfrom trees sprayed with urea or a com-bination of urea and CuEDTA. Stemsfrom trees sprayed with water inNovember had similar N concentra-tions and developed smaller lesionsthan stems from trees in all otherspray treatments. Stems from treessprayed with CuEDTA in Octoberhad lower N concentrations and de-veloped larger lesions than stemsfrom trees sprayed with urea or a com-bination of urea and CuEDTA. Stemsfrom trees sprayed with CuEDTAin November had lower stems Nconcentrations and developed smallerlesions than trees sprayed with a com-bination of urea and CuEDTA. Stems

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Fig. 1. Continued

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from trees sprayed with urea had sim-ilar N concentrations and developedsimilar lesions as trees sprayed with acombination of urea and CuEDTA,regardless of when trees were sprayed.

Lesion size was not correlatedwith stem N concentrations when treeswere sprayed with water or CuEDTAin October (R < 0.350; P > 0.05).Lesions size was positively correlated(P < 0.05) with stem N concentrationswhen trees were sprayed with urea (R =0.700; P < 0.05) or a combinationof urea and CuEDTA (R = 0.573; P <0.05) in October. Lesion size waspositively correlated with stem N con-centrations when trees were sprayedwith water (R = 0.632; P < 0.05) orCuEDTA (R = 0.574; P < 0.05) inNovember, and lesion size was notcorrelated with stem N concentrationswhen trees were sprayed with urea ora combination of urea and CuEDTA inNovember (R < 0.221; P > 0.05).

EXPERIMENT 3. Lesions devel-oped on over 75% of wounds (datanot shown). Trees sprayed with theurea treatment (urea and CuEDTA)in October defoliated before treesthat were sprayed with the urea treat-ment in November (data not shown).

Between October and Novem-ber, stem N concentrations increasedin trees from all spray treatments andlesion size increased between Octo-ber and November when trees weresprayed with water or the urea treat-ment (Fig. 3, A and B). Stems fromtrees sprayed with water had lower Nconcentrations and developed similarsize (October) or larger (November)lesions than stems from trees sprayedwith the urea treatment (Fig. 3, Aand B). Across all spray times andinoculation times, there were positivecorrelations between stem N concen-tration and lesion size when trees

were sprayed with water (R = 0.531,P < 0.05) and the urea (R = 0.465;P < 0.05) treatment. Trees sprayedwith PFOS or a combination of theurea treatment and PFOS developedthe smallest lesions and had similaror higher stem N concentrationsthan trees sprayed with water or theurea treatment (Fig. 3, A and B).There were no significant correlationsbetween stem N concentration andlesion size when trees were sprayedwith PFOS or a combination of theurea treatment and PFOS (R < 0.182;P > 0.05).

Lesion size and stem N concen-trations increased between Octoberand November regardless of whentrees were inoculated (Fig. 3, C andD). Stems from trees inoculated 7 and21 d after spraying in October hadhigher N concentrations and devel-oped similar size lesions than stemsfrom trees inoculated 7 d before and2 d after spraying (Fig. 3, C and D).Stems from trees inoculated 7 d be-fore spraying in November had simi-lar or lower stem N concentrationsand developed larger lesions thantrees inoculated after spraying (Fig.3, C and D). Stems from trees in-oculated 2 d after spraying in Novem-ber had lower stem N concentrationsand developed similar size lesionsas trees inoculated 7 and 21 d afterspraying (Fig. 3, C and D). Therewere positive correlations betweenstem N concentration and lesion sizewhen trees were inoculated beforebeing sprayed with water (R =0.708; P < 0.05) and the urea treat-ment (R = 0.747; P < 0.05). Therewas no correlation between stem Nconcentration and lesion size thenstems were inoculated after beingsprayed with water and the urea treat-ment (R < 0.235; P > 0.05).

DiscussionSTEM N CONCENTRATION AND

SUSCEPTIBILITY. Our results indicatethere are certain conditions that re-sult in positive relationships betweenN concentrations in stems of peartrees and susceptibility to P. syringae.Positive correlations between stemN concentration and lesion size oc-curred for certain treatment combi-nations, time of year, and inoculationtimes in all three experiments. For ex-ample, in Expt. 1, increasing the Nfertigation rate in August, increasedstem N concentration, and increasedsize of lesions on stems; in Expt.2, trees sprayed with CuEDTA inNovember had lower stem N con-centrations and smaller lesions thantrees sprayed with a combination ofurea and CuEDTA; in Expt. 3, treessprayed in November had higherstem N concentrations and developedlarger lesions than trees sprayed inOctober, and in Expt. 3, there werepositive correlations between stem Nconcentration and lesion size whentrees were inoculated before beingsprayed with water or urea. Takentogether, these results suggest thattrees with higher N concentrationswere more susceptible to P. syringae.There are several reports for high Nfertilization rates increasing plantsusceptibility to pathogen infection,including high rates of N fertilizerincreasing disease severity caused byP. infestans on potato [Solanumtuberosum (Herlihy, 1970)], blackshank caused by P. parasitica on to-bacco [Nicotiana tabacum (Apple,1962)], fire blight caused by Erwiniaamylovora (Frecon, 1982), and Septo-ria tritici (Simon et al., 2003) andFusarium head blight caused by F.graminearum and F. culmorum on

Fig. 1. Incidence of Phytophthora syringae infection (A, E, and I), nitrogen (B, F, and J) and amino acid (C, G, and K)concentrations in stems, and size of lesions (D, H, and L) on stems of ‘OHF 97’ pear rootstock grown with different nitrogen(N) rates during August (August N rate), sprayed with urea and chelated copper ethylenediaminetetraacetic acid (CuEDTA) inOctober and November, and inoculated with pathogen 19 Oct. 2002, 7 d before (27 d) or 16 Nov. 2002, 7 d after (+7d) spraytreatments. Stems were collected for analyses on 21 Dec. 2002. August N rate = trees fertigated with 400 mL (13.53 fl oz) of0 (0N), 100 (100N), or 200 (200N) mg�L21 (ppm) N during Aug. 2002; Autumn spray treatment = trees sprayed with water(Water), urea solution (Urea), CuEDTA solution (CUEDTA), or a combination of urea and CuEDTA (Urea + CUEDTA) on26 Oct. and 9 Nov. 2002. (A, E, and I); Disease incidence = percentage of stems with lesions. Columns denoted with the samelower case letters are not significantly different at P > 0.05 as indicated by binomial analyses and multivariate analysis of variance(lesion size and stem concentration.). (B, C, F, G, D, and H) Columns denoted with the same lower case letter are notsignificantly different using Tukey’s honestly significant difference at P < 0.05. (J–L) Significant (P < 0.05) linear (L) contrastsbased on August N rate within an autumn spray treatment denoted by L above column groups. Significant (P < 0.05) differencesin L response to August N rate between autumn spray treatments denoted in superscripts. Columns represent means and errorbars are se (A–D: n = 24; E–H: n = 18; I–L: n = 12); 1 cm = 0.3937 inch, 1 mg�g21 = 1000 ppm.

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wheat [Triticum aestivum (Lemmenset al., 2004)].

Our results suggest that the Nstatus of pear trees is related to sus-ceptibility to P. syringae; however, wedid not always find positive relation-ships between N status and suscepti-bility. There were certain conditionsthat resulted in negative or no rela-tionship between N concentrations instems of pear trees and susceptibilityto P. syringae. For example, in Expt. 1,stems inoculated after autumn spraytreatments developed larger lesionsthan stems inoculated before spraytreatments even though stem N andamino acid concentrations remainedthe same; in Expt. 1, spraying treeswith CuEDTA decreased stem N con-centrations and had no influence onlesion development; in Expt. 2, treessprayed in November developed sim-ilar or lower stem N concentrationsand developed larger lesions thantrees sprayed in October; and in Expt.3, stems from trees sprayed with waterhad lower N concentrations and de-veloped similar or larger lesions thanstems from trees sprayed with a com-bination or urea and CuEDTA. Theseresults indicate that the relationshipbetween N status and susceptibility isinfluenced by other changes in treephysiology during the autumn whenexposed to the pathogen and is notstrictly a function of N status.

There are several examples in ourthree experiments that indicate thatthe relationship between tree N statusand susceptibility is confounded bythe response of trees to different cul-tural practices (e.g., soil N applicationrate, sprays with urea, defoliant, orfungicide, and timing of sprays).In Expt. 1, increasing N fertigationrate in August increased stem N con-centrations and lesion size, but spray-ing trees with urea in the autumnincreased stem N concentrations andhad no influence on lesion size. Theseresults suggest that susceptibility ofpear trees to P. syringae increases withincreasing stem N concentrations butnot when higher N concentrationsare a result of urea sprays. In Expt. 2,spraying trees with CuEDTA loweredstem N concentrations, but lowerN concentrations were associatedwith larger lesions when trees weresprayed in October and with smallerlesions when trees were sprayed inNovember. These results suggest thatdecreased stem N concentrationsresulting from CuEDTA sprays arenot directly related to susceptibilityto P. syringae. Additionally, in Expt.1, when trees were grown with no Nduring August, spraying trees withurea before inoculation increasedstem N concentrations and decreasedthe size of lesions compared withtrees sprayed with water. This result

from trees grown with no N in Au-gust supports anecdotal reports fromsome growers who believe that spray-ing trees with urea in the autumndecreases disease severity caused byP. syringae in the nursery.

There are several examples in ourthree experiments that indicate thatthe relationship between tree N statusand susceptibility is confounded bythe time of year when trees are ex-posed to the pathogen and the po-tential effects of time of year on treephysiology and pathogen activity. Forexample, our results from all experi-ments indicate that trees were moresusceptible to the pathogen in No-vember when stem N concentrationswere similar (Expt. 1), lower (Expt.2), or higher (Expt. 3) than in Octo-ber. Additionally, when stems wereinoculated before being sprayed inNovember (Expt. 3), trees were moresusceptible and had lower stem Nconcentrations than when trees wereinoculated after being sprayed in No-vember. Taken together, our resultsindicate that interactions between en-vironmental conditions (e.g., temper-ature) and physiology of trees wheninoculated with the pathogen (e.g.,dormancy status) change the relation-ship between N status and tree sus-ceptibility to the pathogen.

All of our experiments were doneunder natural environmental condi-tions, and differences in climate andphysiology of trees between years mayhave caused differences in susceptibil-ity associated with tree N concentra-tion. Even though spraying trees withurea increased stem N concentrationsin all years, lesions on trees that re-ceived urea sprays were larger, similar,or smaller than those on trees sprayedwith water. This supports our theorythat N content may be correlated withtree susceptibility, but other factors al-ter plant susceptibility to P. syringae.Additionally, in all of our experiments,lesions that developed from pathogeninoculation in October were smallercompared with lesions that developedfrom inoculation in November. Thissuggests that the level of pathogenactivity or host susceptibility may re-late to temperature.

In all of our experiments, treesinoculated with P. syringae on non-wounded stems showed no symptomsof disease and all wounds inocu-lated with the pathogen showed signsof disease. These results suggest that

Fig. 2. Nitrogen (N) concentrations in stems (A) and the size of lesions (B) causedby Phytophthora syringae infection on stems of ‘OHF 97’ pear rootstock sprayed withurea and chelated copper ethylenediaminetetraacetic acid (CuEDTA) in October orNovember. Trees sprayed with water (Water), urea solution (Urea), CuEDTA, ora combination of urea and CuEDTA (Urea + CuEDTA) on 5 Oct. (Oct.) or 13 Nov.2003 (Nov.) and inoculated with the pathogen 7 d after spraying. Stems were collectedfor analyses 8 weeks after inoculation. Columns represent means and error bars arese (n = 5). Columns denoted with the same lower case letters are not significantlydifferent (lesion size: Kruskal-Wallis test at P < 0.05; stem N: Tukey’s honestlysignificant difference test at P < 0.05); 1 cm = 0.3937 inch, 1 mg�g21 = 1000 ppm.

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wounding may be essential for P.syringae infection of pear stems un-der the environmental conditions inour test system. Others have reportedthat P. syringae was unsuccessful incausing infection to uninjured barkof almond [Prunus dulcis (Bostockand Doster, 1985; De Bruyn, 1924;Linderman, 1986)], and P. syringae caninfect wounds caused by handling orpruning or through leaves and leaf scars(De Bruyn, 1924; Linderman, 1986).In artificial inoculations of P. syringae inrhododendron (Rhododendron spp.),wounds and low temperatures werea prerequisite for infection (Linderman,1986).

The activity of P. syringae is re-stricted to cold climates, and in-creased activity of the pathogencoincides with the dormancy periodof deciduous trees (Duniway, 1983;Erwin and Ribeiro, 1996). Apple[Malus ·domestica (Sewell andWilson, 1973)] and lilac [Syringa vul-garis (De Bruyn, 1924)] were moresusceptible to P. syringae infectionduring the dormant period than inthe actively growing period. The path-ogen activity in apple (Sewell andWilson, 1973) and almond (Bostockand Doster, 1985) was higher incooler months at lower temperatures.This was also reported for the activity

of this pathogen in orchard soil insoutheastern England where the path-ogen was quiescent during warmermonths and active in cooler months(Harris, 1979). In bareroot nurseries,lifting of trees in the PNW coincideswith the greatest activity of P. syringae.If infection occurs during this timeand conditions that are conducivefor pathogen activity follow, the riskof infection could be high, especiallyduring cold storage, because the fun-gus can actively grow at low tempera-tures (Pscheidt and Ocamb, 2002).

UREA SPRAYS AND SUSCEPTIBILITY.In Expt. 2, spraying trees with ureain October increased N concentrationand decreased tree susceptibility toP. syringae, while spraying treeswith urea in November increased Nconcentrations and lesion size. Thiscontrasting relationship between Nconcentration and the size of lesionsbetween October and November sug-gests that time of year plays an im-portant role in tree susceptible to P.syringae beyond the effects of urea onN status.

The results from Expt. 3 supportour hypothesis that the relationshipbetween stem N concentration andsusceptibility varies during the au-tumn. Concentrations of N in stemsfrom trees sprayed with urea in No-vember were greater than in stemsfrom trees sprayed in October, andlesions on stems from trees sprayedwith urea were larger in Novemberthan in October. Compared withtrees sprayed with water, sprayingtrees with urea in October had noinfluence on lesion size and increasedstem N concentration, and sprayingtrees with urea in November de-creased lesions size and increasedstem N concentration. These resultsare important because they indicatethat the timing of urea sprays candifferentially influence tree N concen-trations without altering susceptibil-ity to P. syringae. Similarly, sprayingpear trees with a combination of ureaand CuEDTA had no influence onlesion size regardless of the growingenvironment before or after inocula-tion (Laywisadkul, 2008). These re-sults suggest that the combinedeffects of urea and CuEDTA on stemN concentrations do not increase sus-ceptibility of pear trees to P. syringae.

In general, our results indicatethat spraying trees with urea has noeffect on disease incidence and is

Fig. 3. Nitrogen concentration in stems (A) and the size of lesions (B) caused byPhytophthora syringae infection on stems of ‘OHF 97’ pear rootstock sprayed withurea, chelated copper ethylenediaminetetraacetic acid (CuEDTA), and a fungicidesolution composed of phosphorus acid neutralized with potassium hydroxide[PFOS (PhytoFOS; Sipcam Agro USA, Research Triangle Park, NC)] in October orNovember. Trees sprayed with water (Water), a solution of urea and CuEDTA(Urea), a solution of PFOS (PFOS), or a solution of urea and PFOS (Urea + PFOS)on 22 Oct. (Oct.) or 24 Nov. 2004 (Nov.) and inoculated with pathogen 7 d beforespraying (27 d), or 2, 7, or 21 d (+2d, +7d, or +21d) after spraying. Stems werecollected for analyses 8 weeks after inoculation. Columns represent means and errorbars are se (n = 16). Columns denoted with the same lower case letters are notsignificantly different (lesion size: Kruskal-Wallis test at P < 0.05; stem N: Tukey’shonestly significant difference test at P < 0.05); 1 cm = 0.3937 inch, 1 mg�g21 =1000 ppm.

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not consistently associated with ob-served increases or decreases in sus-ceptibility to P. syringae, even thoughurea sprays increase the concentra-tions of N and amino acids in stems.The relationship between tree suscep-tibility to P. syringae and tree N con-centration may be specific to the formof N (e.g., urea vs. ammonium ni-trate) and the delivery method ortiming of N applications, not on thetree N status per se. Increasing Nsupply from fertigation and sprayingtrees with urea caused similar in-creases in stem N concentration inbench-grafted ‘Fuji’ apple on ‘Malling26’ (‘M26’) rootstock (Cheng andFuchigami, 2002) and June-budded‘Nonpareil’ on ‘Nemaguard’ almondrootstocks (Bi et al., 2003). It is notknown whether similar increases instem N concentration resulting fromspraying apple and almond trees withurea could increase tree susceptibilityto pathogens.

CUEDTA SPRAYS AND SUSCEPTI-

BILITY. Our results suggest sprayingtrees with CuEDTA may increase thesize of lesions caused by P. syringe, butthe effects of CuEDTA on lesion sizewere not related to tree N concentra-tions. Lesions on stems inoculatedbefore trees were sprayed withCuEDTA in Expt. 1 were smaller thanlesions on stems inoculated after treeswere sprayed; however, stems inocu-lated with P. syringae after trees weresprayed had similar N and amino acidconcentrations as stems inoculatedbefore trees were sprayed. This vari-able effect of CuEDTA on diseaseseverity by P. syringae suggests thatother factors, such as environment(e.g., temperatures) or stage of plantdevelopment (e.g., dormancy devel-opment), may be involved in the re-lationship between CuEDTA andsusceptibility.

Spraying apple trees withCuEDTA can cause >80% defoliationwithin 6 d of application and results inlow N recovery from leaves comparedwith natural defoliation (Guak et al.,2001). Spraying almond and appletrees with CuEDTA in October hasbeen shown to decrease stem N con-centrations (Bi et al., 2005; Guak et al.,2001). Similar effects of CuEDTA ondefoliation and loss of N have beenreported for almond nursery trees (Biet al., 2005). The effects of CuEDTAin our studies were not always consis-tent with reported effects of CuEDTA

on defoliation; CuEDTA did notalways cause premature defoliationbefore natural N translocation fromleaves into tree stems. The poor effi-ciency of CuEDTA as a defoliant wassupported by its lack of consistent in-fluence on stem N concentrations inour experiments. Effects of CuEDTAon tree susceptibility to P. syringae inour experiments could not be directlyrelated with stem N concentrations.

In our experiments, defoliationafter spraying container-grown peartrees with CuEDTA took longer thandefoliation in the experiments de-scribed above with apple and almond.With container-grown pear trees, it ispossible that this longer time for de-foliation resulted in mobilization ofN back to stems and the other partsof the trees. Also, because only Nconcentrations in pear stems wereanalyzed, it is possible that N concen-trations in roots were significantlydecreased by spraying trees withCuEDTA, similar to the results de-scribed by Guak et al. (2001). In Expt.2, spraying pear trees with CuEDTAin October did not decrease stem Nconcentrations, but spraying treeswith CuEDTA in November de-creased N concentrations. The differ-ences in concentration and timing ofapplication between our studies andthose from other studies may accountfor the different responses in N con-centration to CuEDTA.

COMBINED UREA AND CUEDTASPRAYS AND SUSCEPTIBILITY. Our re-sults suggest that timing of spraytreatments with urea and CuEDTAdifferentially influenced tree suscepti-bility to P. syringae, and the responsedepends on when trees were inocu-lated with the pathogen. In Expt. 3,when trees were sprayed in October,time of inoculation (e.g., before orafter trees were sprayed) had no in-fluence on lesion size. When treeswere sprayed in November, stem le-sions were largest when trees wereinoculated before being sprayed. Thissuggests that sprays may physicallyor chemically alter tree susceptibilitybefore pathogen presence, resultingin less disease. This result supportsanecdotal reports from growers whobelieve using a combined spray ofurea and CuEDTA decreases inci-dence of P. syringae in the nursery.

In our experiments, trees sprayedwith a combination of urea andCuEDTA in November had similar

stem N concentrations as trees sprayedwith only urea and greater stem Nconcentrations than trees sprayed withonly CuEDTA. Similar amelioratingeffects of urea on N status of treessprayed with CuEDTA have beenreported by others (Bi et al., 2005;Guak et al., 2001). In our study, thiseffect was only observed when treeswere sprayed in November and notOctober. Using similar concentrationsof urea and CuEDTA, apple trees weresprayed two times with urea followedby one spray with CuEDTA in thework of Guak et al. (2001), andalmond trees were sprayed with ureafollowed by a combined spray treat-ment of urea and CuEDTA by Bi et al.(2005). We used a single foliar appli-cation of urea + CuEDTA in our study,which may account for the lack ofresponse in stem N concentration tothe combined urea + CuEDTA spray.Splitting two urea applications, as de-scribed for almond (Bi et al., 2005),with a pretreatment of urea followedby the combination of urea andCuEDTA is a more useful strategyfor improving N content in Octobercompared with a single spray with acombination of urea and CuEDTA.

Our results from Expt. 3 supportour hypothesis that the effects of ureaand CuEDTA on susceptibility to P.syringae may be a function of theinteraction between environment andplant development. The N concentra-tions in pear stems increased fromOctober to the end of the experiment.Trees sprayed with a combination ofurea and CuEDTA in October defo-liated before trees that were sprayedwith a combination of urea andCuEDTA in November. IncreasingN concentrations during the autumnis a result of trees moving N fromleaves to storage locations in the stemsand roots before leaf abscission oc-curs (Bi et al., 2003; Cheng andFuchigami, 2002). Compared withtrees sprayed with water, trees sprayedwith a combination of urea andCuEDTA in October and Novemberhad higher N concentrations in stems;however, the effects of urea on Nconcentrations in stems was less whentrees were sprayed in November thanin October. Between the October andNovember spray treatments, theremay have been N mobilization fromleaves to stems, resulting in higher Nconcentrations in stems of treessprayed with water. The increase in N

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concentrations as trees sprayed withwater became more dormant coin-cided with increased susceptibility toP. syringae. This supports our previousresults showing that susceptibility ofpear trees to P. syringae increases astrees become more dormant in the au-tumn and early winter (Laywisadkul,2008).

Our results indicate that the tim-ing of inoculation in relation to thetiming of urea and CuEDTA spraysplays a role in disease severity and isindependent of the effects of urea andCuEDTA on tree N concentrations.Therefore, differences in tree suscep-tibility to P. syringae before and afterspray treatments were not related toconcentrations of N and amino acidsin stems. Susceptibility of pear trees toP. syringae increases as trees becomemore dormant in the autumn andearly winter (Laywisadkul, 2008). Itis possible that differences in lesiondevelopment between the two inocu-lation times were the result of envi-ronmental differences between thetwo inoculation times and influenceon tree dormancy and disease severity.

C H E M I C A L C O N T R O L A N D

SUSCEPTIBILITY. Fungicides used inour experiments effectively controlledactivity of P. syringae when applied7 and 2 d before inoculation. Fungi-cides containing fosetyl-Al (Expt. 2)and phosphorous acid (Expt. 3) de-creased disease incidence and severityof P. syringae infection on pear stemsin our experiments with little (Expt.3) or no (Expt. 2) influence on stemN concentrations.

In Expt. 2, spraying trees witha fosetyl-Al–containing fungicidesdecreased disease severity without al-tering N concentrations in stems ordefoliation. Others have also reportedfosetyl-Al has good activity against P.cactorum (Bielenin and Jones, 1988;Ellis et al., 1998; Orlikowski et al.,1986; Thomidis and Elena, 2001),P. cinnamomi (Coffey et al., 1984;Darvas et al., 1984; Matheron andMircetich, 1985; Pegg et al., 1987),P. citrophthora (Farih et al., 1981;Matheron and Mircetich, 1985), andP. syringae (Doster and Bostock,1988). Our results indicate that usingfosetyl-Al–containing fungicides incombination with urea or CuEDTAsprays is a compatible strategy forreducing disease caused by P. syringaewithout impacting growers’ objectiveof increasing tree N concentrations

with urea sprays or enhancing earlydefoliation with CuEDTA.

In Expt. 3, trees sprayed witha phosphorous acid-containing fungi-cide in October had higher stem Nconcentrations than trees sprayedwith water. It is possible the Octoberapplication of fungicide in Expt. 3 mayhave had a growth-stimulating influ-ence on trees, resulting in increased Nconcentrations in stems. Phosphite hasbeen reported as a nutritional andfungicidal material (Guest and Grant,1991; Rickard, 2000; Varadarajanet al., 2002). Phosphite is not used asa substrate for phosphate-dependantenzymes because it is not convertedto phosphate in trees (Carswell et al.,1996). However, it is not known howphosphite may alter N concentrationwhen applied with urea + CuEDTA.Phosphite application to citrus (Citrusspp.) can cause similar increases ingrowth and fruit set similar to foliarsprays of urea (Lovatt, 1999). It ispossible that the October applicationof fungicide in Expt. 3 may have had aphytotoxic effect on pear trees, causingpremature leaf senescence and earlymobilization of N from leaves backinto stems. Although phosphite hasbeen described as having low toxicityto plants (Guest and Grant, 1991),there are a number of reports of thedevelopment of phytotoxicity symp-toms after foliar application of phos-phite, including leaf burn (Walker,1989; Wicks and Hall, 1988).

There are numerous reports ofphosphorous acid as an effective con-trol against P. cambivora in cherry[Prunus avium (Wicks and Hall,1988)], P. cinnamomi on pineapple[Ananas comosus (Rohrback andSchenck, 1985)], eucalyptus [Euca-lyptus spp. (Pilbeam et al., 2000;Wilkinson et al., 2001)], and avocado[Persea americana (Pegg et al.,1987)], P. citrophthora in citrus(Afek and Sztejnberg, 1989), and P.palmivora in cacao [Theobroma cacao(Holderness, 1990)]. Our results in-dicate that using phosphorous acid incombination with urea or CuEDTAsprays is a compatible strategy forreducing disease caused by P. syringaeand the timing of phosphorous acidsprays in relation to urea or CuEDTAsprays will not influence its effects ondisease control.

CONCLUSIONS. Spraying pear‘OHF 97’ rootstock in the autumnwith urea, defoliants, or fungicides

containing fosetyl-Al or phosphitemay influence tree N concentration,but their effects on N concentrationare not directly related to susceptibil-ity to P. syringae. Spraying pear treeswith a combination of urea andCuEDTA after terminal buds haveset in early autumn (October inPNW) can benefit nurserymen be-cause the pathogen is less active inwarm dry environments and thetrees are better able to heal woundscaused by defoliation or chemicaltreatments. Trees sprayed in Octoberhave lower N reserves compared withtrees sprayed in November or natu-rally defoliated trees; therefore, spray-ing trees in October will not have asmuch of a positive influence on treegrowth the following year. Addition-ally, spraying trees with a combinationof urea and CuEDTA with phospho-nate-containing fungicides in earlyautumn can be of benefit for earlyharvesting and preventing the con-tamination and/or infection of P.syringae in the field or storage.

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