scholarly journals Bacterial Canker Disease of Wild Actinidia Plants as the Infection Source of Outbreak of Bacterial Canker of Kiwifruit Caused by Pseudomonas syringae pv. actinidiae.

1992 ◽  
Vol 58 (3) ◽  
pp. 426-430 ◽  
Author(s):  
Kinji USHIYAMA ◽  
Nobuhiro KITA ◽  
Kazuo SUYAMA ◽  
Nobuo AONO ◽  
Junko OGAWA ◽  
...  
2014 ◽  
Vol 67 ◽  
pp. 34-40 ◽  
Author(s):  
K.J. Froud ◽  
N. Cogger ◽  
R.M. Beresford

Bacterial canker disease caused by a virulent strain of Pseudomonas syringae pv actinidiae (PsaV) has affected kiwifruit vines in New Zealand since 2010 This study investigated the association of PsaV with productivity within Hayward and Hort16A varieties PsaV infection status and date of diagnosis for 3309 infected orchards were provided by Kiwifruit Vine Health while Zespri provided productivity data Linear regression models were constructed to determine the relationship between production and PsaV infection in Hayward and Hort16A orchards Results showed a significant relationship between the numbers of weeks PsaV was detected in Hort16A orchards and a reduction in productivity This was likely due to the removal of Hort16A vines or productive areas of canopy in response to the presence of severe symptoms within an orchard A similar significant relationship was also found in Hayward orchards although the reduction in productivity was smaller and took longer to develop than in Hort16A


2021 ◽  
Vol 37 (5) ◽  
pp. 489-493
Author(s):  
Young Sun Lee ◽  
Gyoung Hee Kim ◽  
Young Jin Koh ◽  
Jae Sung Jung

Bacterial canker is a devastating disease of kiwifruit caused by the bacterium <i>Pseudomonas syringe</i> pv. <i>actinidiae</i>. Canker disease of kiwifruit in Korea has been controlled using streptomycin for more than two decades. Four streptomycin-resistant strains, belonging to biovar 2, which are found only in Korea, were collected between 2013 and 2014 from different orchards located in Jeju, Korea. The genetic background for streptomycin resistance among <i>P. syringe</i> pv. <i>actinidiae</i> strains were determined by examining the presence of <i>strA</i>-<i>strB</i> or <i>aadA</i>, which are genes frequently found in streptomycin-resistant bacteria, and a point mutation at codon 43 in the <i>rpsL</i> gene. All four streptomycin-resistant strains of <i>P. syringe</i> pv. <i>actinidiae</i> investigated in this study contained <i>strA</i>-<i>strB</i> as a resistant determinant. The presence of the <i>aadA</i> gene and a mutation in codon 43 of the <i>rpsL</i> gene was not identified.


2021 ◽  
Vol 9 (6) ◽  
pp. 1328
Author(s):  
Helen C. Neale ◽  
Michelle T. Hulin ◽  
Richard J. Harrison ◽  
Robert W. Jackson ◽  
Dawn L. Arnold

Bacterial canker of Prunus, affecting economically important stone fruit crops including cherry, peach, apricot and plum, is caused by the plant pathogen Pseudomonas syringae (P.s.). Strains from two pathovars—P.s. pv. syringae (Pss) and P.s. pv. morsprunorum race 1 (PsmR1) and 2 (PsmR2)—in three phylogenetically distant clades have convergently evolved to infect Prunus. The bacteria enter woody tissues through wounds and leaf scars, causing black necrotic cankers. Symptoms are also produced on blossom, fruit and leaves. Little is known about the mechanisms P.s. uses to colonise tree hosts such as Prunus. Here, we created transposon (Tn) mutant libraries in one strain of P.s. from each of the three clades and screened the mutants on immature cherry fruit to look for changes in virulence. Mutants (242) with either reduced or enhanced virulence were detected and further characterised by in vitro screens for biofilm formation, swarming ability, and pathogenicity on leaves and cut shoots. In total, 18 genes affecting virulence were selected, and these were involved in diverse functions including motility, type III secretion, membrane transport, amino acid synthesis, DNA repair and primary metabolism. Interestingly, mutation of the effector gene, hopAU1, led to an increase in virulence of Psm R2.


Antibiotics ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 554
Author(s):  
Yu-Rim Song ◽  
Nguyen Trung Vu ◽  
Jungkum Park ◽  
In Sun Hwang ◽  
Hyeon-Ju Jeong ◽  
...  

Pseudomonas syringae pv. actinidiae (Psa) is a Gram-negative bacterium that causes bacterial canker disease in kiwifruit. Copper or antibiotics have been used in orchards to control this disease, but the recent emergence of antibiotic-resistant Psa has called for the development of a new control agent. We previously reported that the bacteriophage (or phage) PPPL-1 showed antibacterial activity for both biovar 2 and 3 of Psa. To investigate the possibility of PPPL-1 to control bacterial canker in kiwifruit, we further tested the efficacy of PPPL-1 and its phage cocktail with two other phages on suppressing disease development under greenhouse conditions using 6 weeks old kiwifruit plants. Our results showed that the disease control efficacy of PPPL-1 treatment was statistically similar to those of phage cocktail treatment or AgrimycinTM, which contains streptomycin and oxytetracycline antibiotics as active ingredients. Moreover, PPPL-1 could successfully kill streptomycin-resistant Psa isolates, of which the treatment of BuramycinTM carrying only streptomycin as an active ingredient had no effect in vitro. The phage PPPL-1 was further characterized, and stability assays showed that the phage was stable in the field soil and at low temperature of 0 ± 2 °C. In addition, the phage could be scaled up quickly up to 1010 pfu/mL at 12 h later from initial multiplicity of infection of 0.000005. Our results indicate that PPPL-1 phage is a useful candidate as a biocontrol agent and could be a tool to control the bacterial canker in kiwifruit by Psa infection in the field conditions.


2020 ◽  
Author(s):  
Jay Jayaraman ◽  
Minsoo Yoon ◽  
Emma R. Applegate ◽  
Erin A. Stroud ◽  
Matthew D. Templeton

SummaryPseudomonas syringae pv. actinidiae ICMP 18884 biovar 3 (Psa3) produces necrotic lesions during infection of its kiwifruit host. Bacterial growth in planta and lesion formation are dependent upon a functional type III secretion system (T3S), which translocates multiple effector proteins into host cells. Associated with the T3S locus is the conserved effector locus (CEL), which has been characterised and shown to be essential for the full virulence in other P. syringae pathovars. Two effectors at the CEL, hopM1 and avrE1, as well as an avrE1-related non-CEL effector, hopR1, have been shown to be redundant in the model pathogen P. syringae pv. tomato DC3000 (Pto), a close relative of Psa. However, it is not known whether CEL-related effectors are required for Psa pathogenicity. The Psa3 allele of hopM1, and its associated chaperone, shcM, have diverged significantly from their orthologs in Pto. Furthermore, the CEL effector hopAA1-1, as well as a related non-CEL effector, hopAA1-2, have both been pseudogenised. We have shown that HopM1 does not contribute to Psa3 virulence due to a truncation in shcM, a truncation conserved in the Psa lineage, likely due to the need to evade HopM1-triggered immunity in kiwifruit. We characterised the virulence contribution of CEL and related effectors in Psa3 and found that only avrE1 and hopR1, additively, are required for in planta growth and lesion production. This is unlike the redundancy described for these effectors in Pto and indicates that these two Psa3 genes are key determinants essential for kiwifruit bacterial canker disease.


2015 ◽  
Vol 3 (5) ◽  
Author(s):  
Matthew D. Templeton ◽  
Benjamin A. Warren ◽  
Mark T. Andersen ◽  
Erik H. A. Rikkerink ◽  
Peter C. Fineran

Pseudomonas syringae pv. actinidiae is the causal agent of bacterial canker of kiwifruit, a disease that has rapidly spread worldwide. We have fully sequenced and assembled the chromosomal and plasmid DNA from P. syringae pv. actinidiae ICMP 18884 using the PacBio RS II platform.


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