Epidemiological Relations of the Pseudomonad Pathogens of Deciduous Fruit Trees

Crosse, J. E.

doi:10.1146/annurev.py.04.090166.001451

Cited by 65 publications

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“…fraxini does not appear to be related to the presence of rapid diffusing toxins and bacterial activity occurs in the growing season when host defence reactions take place, the slow development of bacterial protuberances becomes evident. A strong bacterial proliferation in spring is also observed in various other bacterial diseases of trees (CROSSE 1966;KONING 1938;RIDB and RIDB 1978).…”

Section: Discussionmentioning

confidence: 87%

The bacterial disease of ash (Fraxinus excelsior), caused by Pseudomonas syringae subsp. savastanoi pv. fraxini III. Pathogenesis

Janse

1982

European Journal of Forest Pathology

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The pathogenesis of the bacterial disease of ash, caused by Pseudomonas syringae subsp. savastanoi pv. fraxini is macroscopically studied and by means of light-and electron-microscopy. Anatomical changes of the host tissue caused by l? syringae subsp. sawastanoipv. oleae and those caused by the fungus Nectria galli ens are compared. Pv. fraxini is a necrotrophic parasite, causing slowly growing necrotic bark swelfings characterized by extensive periderm formation. Pv. oleae causes parenchymatous galls on ash and N. galligena a real canker. The new name "bacterial knot" is proposed for the disease caused by pv.fraxini. Material and methodsMaterial examined: Fraxinus excelsior L. Macroscopic observationsMore than 200 transverse sections of material naturally infected by pv. fraxini, and by N . galligena were macroscopically compared and studied. U. S.In this paper the pathogenesis of the bacterial disease of ash, caused b Pseudomonas syrin ae subsp. means of light-and electron-microscopy, Tissue changes in ash evoked by pv. frmini were compared with those caused by the related P. syringa subsp. savastanoi pv. oleae and the fungus Nectria alligena.to the bark showing bacterial cavities, hyperplasy, hypertro hy, marked peridem formation and caused by N . galligena do not develop. Secondary fungi are found following a c t e d Invasion. Pv. fraxini is a necrotrophic parasite and is passively spreading through the intercellular spaces. Bacterial progression, which appears to be confined to the growing season of ash, IS slow contrary to that of N. galligena .The name "bacterial knot" is proposed instead of "bacterial canker", the latter being a misapplication. savastanoi pv. fraxini is described. Anatomical observations were peLrmed macroscopic f ly and by It is shown that characteristic excrescences (protuberances), caused by pv.fraxini are main f y limited necrosis. It is also demonstrated that large parenchymatous g a f Is, as caused by r. oleae or cankers as

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Section: Discussionmentioning

confidence: 87%

The bacterial disease of ash (Fraxinus excelsior), caused by Pseudomonas syringae subsp. savastanoi pv. fraxini III. Pathogenesis

Janse

1982

European Journal of Forest Pathology

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“…Pseudomonas syringae causes damages on pear buds, flowers, leaves and fruits; only in very cold winter conditions can cankers on trunks and branches be observed (Wilson 1936;Crosse 1966;Jones and Aldwinkle 1990). In Belgium and in other countries, economically important diseases are blossom blast and bud deads during winter (Clara 1932;Wormald 1946;Parker and Burkholder 1950;Deckers and Daemen 1991;Montesinos and Vilardell 1991).…”

Section: Discussionmentioning

confidence: 99%

Pathogenicity and aggressiveness in populations of Pseudomonas syringae from Belgian fruit orchards

et al. 2009

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The pathogenicity of 99 Belgian Pseudomonas syringae strains representative of the genetic diversity encountered in Belgian fruit orchards was evaluated by using 17 pathogenicity tests conducted on pear, cherry, plum, lilac, sugar beet and wheat. The P. syringae pv. morsprunorum strains were pathogenic to stone fruit species but the race 1 strains possessing the cfl gene involved in coronatine production were pathogenic in more tests than those lacking the gene. Also, sweet cherry twigs were a better material to detect pathogenic strains of race 1 and sour cherry twigs of race 2, which accorded with race 2 presence in sour cherry orchards in Belgium. Three groups were defined in the pv. syringae based on pathogenicity. One group pathogenic in 71.1% of the tests and to lilac included toxic lipodesipeptideproducing (TLP+) strains. The second group pathogenic in 26.8% of the tests and non-pathogenic to lilac included TLP+ strains. The thirth group pathogenic in 9.1% of the tests and almost specifically pathogenic to pear included TLP− strains. The three groups were genetically heterogeneous. Although strain-host relationships were noted within the pv. syringae, aptata and atrofaciens when considering the strain origins, such relationships were not found in the pathogenicity tests, suggesting that pathogenicity tests could probably not reproduce all the aspects of the host-pathogen interactions. None of the pathogenicity tests was able to provide all the information provided by the complete study. A test on pear buds indicated that strains different from the pv. syringae were pathogenic to pear.

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“…These inoculations differed from leaf-scar inoculations in three major respects. The effective inoculum dose was probably massive compared with that in leaf-scar infections (Crosse, 1966) ; the inoculations resulted in mechanical damage to tissues at the site of infection; and they were made at a time (December) when branch tissues were fully dormant and in their most susceptible condition (Shanmuganathan, I 962). It is possible that a hypersensitivity reaction was induced by heterologous bacteria in wound inoculations but was not effective against them at the very high inoculum doses employed.…”

Section: J E C R O S S E a N D C M E G A R R E T Tmentioning

confidence: 99%

Pathogenicity of Pseudomonas morsprunorum in Relation to Host Specificity

Crosse

Garrett

1970

Journal of General Microbiology

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S U M M A R YDifferences in phage type between plum and cherry strains of Pseudomonas morspruiiorum were stable during passage through the homologous and heterologous hosts. In experiments controlled by phage typing reisolates from lesions, both strains were specific for the homologous plant when inoculated into leaves at low concentrations (< 105/ml.) but not at high concentrations (> io6/ml.). No specificity was observed in wound inoculations of branches made during the winter.Autumn inoculation of cherry leaf scars with cherry strains resulted in severe disease, with a dose response type of relationship between inoculum concentration and infection. Plum strains were ineffective through cherry leaf scars and inhibited infection by cherry strains when present in the same inoculum. The inhibitory effect was not observed with plum strains killed by heat or streptomycin, or with plum strains inoculated live in the presence of bacteriostatic levels of streptomycin.

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Epidemiological Relations of the Pseudomonad Pathogens of Deciduous Fruit Trees

Cited by 65 publications

References 0 publications

The bacterial disease of ash (Fraxinus excelsior), caused by Pseudomonas syringae subsp. savastanoi pv. fraxini III. Pathogenesis

The bacterial disease of ash (Fraxinus excelsior), caused by Pseudomonas syringae subsp. savastanoi pv. fraxini III. Pathogenesis

Pathogenicity and aggressiveness in populations of Pseudomonas syringae from Belgian fruit orchards

Pathogenicity of Pseudomonas morsprunorum in Relation to Host Specificity

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