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Trevor A. Jackson - One of the best experts on this subject based on the ideXlab platform.
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bacteria for use against soil inhabiting insects
Manual of Techniques in Invertebrate Pathology (Second Edition), 2012Co-Authors: Albrecht M Koppenhofer, Trevor A. Jackson, Michael G KleinAbstract:Very few bacteria are available against soil-inhabiting pests because only highly co-evolved or unique pathogenic bacteria seems to be able to overcome the defenses of soil-dwelling pests. The bacteria that are available are almost exclusively used against white grubs, larvae of beetles in the family Scarabaeidae. This chapter concentrates on scarab-active and tipulid-active strains of Bacillus thuringiensis; Paenibacillus popilliae , and P. lentimorbus which cause milky Disease in scarab larvae; and strains of Serratia entomophila and S. proteamaculans which cause Amber Disease in scarab larvae. The chapter describes methods of isolation, identification, in vivo and in vitro propagation, laboratory and greenhouse bioassays, and preservation for these pathogens.
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Serratia entomophila inoculation causes a defect in exocytosis in Costelytra zealandica larvae.
Insect molecular biology, 2008Co-Authors: H.s. Gatehouse, Laurence N. Gatehouse, Trevor A. Jackson, Sean D. G. Marshall, Robert M. Simpson, John T. ChristellerAbstract:Rapid elimination of midgut luminal proteinase activity and gut clearance are the two major symptoms of Amber Disease in Costelytra zealandica larvae because of the three-subunit protein toxin complex produced in Serratia entomophila and Serratia proteamaculans. Quantitative PCR analysis of mRNA from the major serine proteinase gene families showed that loss of proteinase activity did not result from transcriptional downregulation. Unexpectedly, protein levels and rates of protein synthesis increased, rather than decreased, in the midgut of Diseased insects. Proteomic analysis of midgut tissues showed marked differences between healthy and Diseased midguts. Large increases in soluble forms of both actin and tubulin were identified from 2D-gels, together with concurrent decreases in the levels of polymeric actin-associated proteins: actin depolymerizing factor and cyclophilin. These results suggest that the Serratia toxin acts to cause degradation of the cytoskeletal network and prevent secretion of midgut gut digestive proteinases as both the actin cytoskeleton and microtubules are involved in exocytosis. Proteinases synthesized in the Diseased midgut must be rapidly degraded because they do not accumulate in an inactive form.
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Induced expression of the Serratia entomophila Sep proteins shows activity towards the larvae of the New Zealand grass grub Costelytra zealandica.
FEMS microbiology letters, 2007Co-Authors: Mark R. H. Hurst, Binglin Tan, Sandra M. Jones, Trevor A. JacksonAbstract:Serratia entomophila and Serratia proteamaculans cause Amber Disease of the grass grub Costelytra zealandica (Coleoptera: Scarabaeidae). Three genes required for virulence, sepABC, are located on a large plasmid, pADAP. The translated products of the sep genes are members of the toxin complex (Tc) family of insecticidal toxins that reside in the genomes of some Enterobacteriaceae. Each of the sep genes was placed either singly or as various combinations under the control of an inducible arabinose promoter, allowing their inductive expression. Western Immunoblot confirmed that each of the Sep proteins migrated at their predicted size on sodium dodecyl sulphate-polyacrylamide gel electrophoresis gel. Bioassays of sonicated filtrates derived from the various arabinose-induced para-SEP constructs showed that only when sepA, sepB and sepC were coexpressed were Amber Disease symptoms observed in grass grub larvae. Fourteen days after ingestion of the Sep protein filtrate, approximately 64% of the larvae reverted from a Diseased to a healthy phenotype. Redosing the revertents with a fresh Sep protein filtrate reinitiated the Amber pathotype, indicating that the Sep proteins are needed to be continuously present to exert an effect.
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Virulence of Serratia Strains against Costelytra zealandica
Applied and environmental microbiology, 2006Co-Authors: Binglin Tan, Trevor A. Jackson, Mark R. H. HurstAbstract:Strains of Serratia spp. showed a high level of virulence when injected into the hemocoel of larvae Costelytra zealandica, with Serratia entomophila, S. plymuthica, and S. marcescens showing significantly higher virulence than S. proteamaculans. Toxicity was independent of the Amber Disease-causing plasmid pADAP, suggesting a generalized Serratia toxin.
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Cloning Serratia entomophila Antifeeding Genes—a Putative Defective Prophage Active against the Grass Grub Costelytra zealandica
Journal of bacteriology, 2004Co-Authors: Mark R. H. Hurst, Travis R. Glare, Trevor A. JacksonAbstract:Serratia entomophila and Serratia proteamaculans (Enterobacteriaceae) cause Amber Disease in the grass grub Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. Larval Disease symptoms include cessation of feeding, clearance of the gut, Amber coloration, and eventual death. A 155-kb plasmid, pADAP, carries the genes sepA, sepB, and sepC, which are essential for production of Amber Disease symptoms. Transposon insertions in any of the sep genes in pADAP abolish gut clearance but not cessation of feeding, indicating the presence of an antifeeding gene(s) elsewhere on pADAP. Based on deletion analysis of pADAP and subsequent sequence data, a 47-kb clone was constructed, which when placed in either an Escherichia coli or a Serratia background exerted strong antifeeding activity and often led to rapid death of the infected grass grub larvae. Sequence data show that the antifeeding component is part of a large gene cluster that may form a defective prophage and that six potential members of this prophage are present in Photorhabdus luminescens subsp. laumondii TTO1, a species which also has sep gene homologues.
Mark R. H. Hurst - One of the best experts on this subject based on the ideXlab platform.
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serratia proteamaculans strain agr96x encodes an antifeeding prophage tailocin with activity against grass grub costelytra giveni and manuka beetle pyronota species larvae
Applied and Environmental Microbiology, 2018Co-Authors: Mark R. H. Hurst, Amy K Beattie, Sandra C Jones, Aurelie Laugraud, Chikako Van Koten, Lincoln HarperAbstract:A highly virulent Serratia proteamaculans strain, AGR96X, exhibiting specific pathogenicity against larvae of the New Zealand grass grub (Costelytra giveni; Coleoptera: Scarabaeidae) and the New Zealand manuka beetle (Pyronota festiva and P. setosa; Coleoptera: Scarabaeidae), was isolated from a Diseased grass grub larva. A 12-day median lethal dose of 4.89 × 103 ± 0.92 × 103 cells per grass grub larva was defined for AGR96X, and death occurred within 5 to 12 days following the ingestion of a high bacterial dose. During the infection period, the bacterium rapidly multiplied within the insect host and invaded the hemocoel, leading to a mean bacterial load of 8.2 × 109 cells per larva at 6 days postingestion. Genome sequencing of strain AGR96X revealed the presence of a variant of the Serratia entomophila antifeeding prophage (Afp), a tailocin designated AfpX. Unlike Afp, AfpX contains two Afp16 tail-length termination protein orthologs and two putative toxin components. A 37-kb DNA fragment encoding the AfpX-associated region was cloned, transformed into Escherichia coli, and fed to C. giveni and Pyronota larvae, causing mortality. In addition, the deletion of the afpX15 putative chaperone component abolished the virulence of AGR96X. Unlike S. entomophila Afp, the AfpX tailocin could be induced by mitomycin C. Transmission electron microscopy analysis revealed the presence of Afp-like particles of various lengths, and when the purified AfpX tailocin was fed to grass grub or manuka beetle larvae, they underwent phenotypic changes similar to those of larvae fed AGR96X.IMPORTANCESerratia proteamaculans strain AGR96X shows dual activity against larvae of endemic New Zealand pasture pests, the grass grub (Costelytra giveni) and the manuka beetle (Pyronota spp.). Unlike Serratia entomophila, the causal agent of Amber Disease, which takes 3 to 4 months to kill grass grub larvae, AGR96X causes mortality within 5 to 12 days of ingestion and invades the insect hemocoel. AGR96X produces a unique variant of the S. entomophila antifeeding prophage (Afp), a cell-free phage-like entity that is proposed to deliver protein toxins to the grass grub target site, causing a cessation of feeding activity. Unlike other Afp variants, AGR96X Afp, named AfpX, contains two tail-length termination proteins, resulting in greater variability in the AfpX length. AfpX shows dual activity against both grass grub and manuka beetle larvae. AGR96X is a viable alternative to S. entomophila for pest control in New Zealand pasture systems.
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nucleotide sequence of the serratia entomophila plasmid padap and the serratia proteamaculans pu143 plasmid virulence associated region
Plasmid, 2011Co-Authors: Mark R. H. Hurst, Anette S Becher, Maureen OcallaghanAbstract:Some strains of Serratia entomophila and S. proteamaculans cause Amber Disease of the New Zealand grass grub Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. The Disease determinants of S. entomophila, are encoded on a 153,404-bp plasmid, termed pADAP for Amber Disease associated plasmid. The S. proteamaculans strain 143 (Sp143) exhibits an unusual pathotype, where only 60–70% of C. zealandica larvae infected with the bacterium succumb to Disease. DNA sequence analysis of the Sp143 pU143 virulence associated region identified high DNA similarity to the pADAP sep virulence associated region, with DNA sequence variation in the sepA gene and the variable region of the sepC component. No pADAP anti-feeding prophage orthologue was detected in the Sp143 genome. The region of pADAP replication was cloned and found to replicate in S. entomophila but not in Escherichia coli. DNA sequence analysis of the plasmid pSG348 repA gene from the French isolate of Serratia grimesii, identified 93% DNA identity to the pADAP repA gene. A comparison of the pU143 virulence associated region with the completed pADAP nucleotide sequence is given.
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Induced expression of the Serratia entomophila Sep proteins shows activity towards the larvae of the New Zealand grass grub Costelytra zealandica.
FEMS microbiology letters, 2007Co-Authors: Mark R. H. Hurst, Binglin Tan, Sandra M. Jones, Trevor A. JacksonAbstract:Serratia entomophila and Serratia proteamaculans cause Amber Disease of the grass grub Costelytra zealandica (Coleoptera: Scarabaeidae). Three genes required for virulence, sepABC, are located on a large plasmid, pADAP. The translated products of the sep genes are members of the toxin complex (Tc) family of insecticidal toxins that reside in the genomes of some Enterobacteriaceae. Each of the sep genes was placed either singly or as various combinations under the control of an inducible arabinose promoter, allowing their inductive expression. Western Immunoblot confirmed that each of the Sep proteins migrated at their predicted size on sodium dodecyl sulphate-polyacrylamide gel electrophoresis gel. Bioassays of sonicated filtrates derived from the various arabinose-induced para-SEP constructs showed that only when sepA, sepB and sepC were coexpressed were Amber Disease symptoms observed in grass grub larvae. Fourteen days after ingestion of the Sep protein filtrate, approximately 64% of the larvae reverted from a Diseased to a healthy phenotype. Redosing the revertents with a fresh Sep protein filtrate reinitiated the Amber pathotype, indicating that the Sep proteins are needed to be continuously present to exert an effect.
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Virulence of Serratia Strains against Costelytra zealandica
Applied and environmental microbiology, 2006Co-Authors: Binglin Tan, Trevor A. Jackson, Mark R. H. HurstAbstract:Strains of Serratia spp. showed a high level of virulence when injected into the hemocoel of larvae Costelytra zealandica, with Serratia entomophila, S. plymuthica, and S. marcescens showing significantly higher virulence than S. proteamaculans. Toxicity was independent of the Amber Disease-causing plasmid pADAP, suggesting a generalized Serratia toxin.
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Cloning Serratia entomophila Antifeeding Genes—a Putative Defective Prophage Active against the Grass Grub Costelytra zealandica
Journal of bacteriology, 2004Co-Authors: Mark R. H. Hurst, Travis R. Glare, Trevor A. JacksonAbstract:Serratia entomophila and Serratia proteamaculans (Enterobacteriaceae) cause Amber Disease in the grass grub Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. Larval Disease symptoms include cessation of feeding, clearance of the gut, Amber coloration, and eventual death. A 155-kb plasmid, pADAP, carries the genes sepA, sepB, and sepC, which are essential for production of Amber Disease symptoms. Transposon insertions in any of the sep genes in pADAP abolish gut clearance but not cessation of feeding, indicating the presence of an antifeeding gene(s) elsewhere on pADAP. Based on deletion analysis of pADAP and subsequent sequence data, a 47-kb clone was constructed, which when placed in either an Escherichia coli or a Serratia background exerted strong antifeeding activity and often led to rapid death of the infected grass grub larvae. Sequence data show that the antifeeding component is part of a large gene cluster that may form a defective prophage and that six potential members of this prophage are present in Photorhabdus luminescens subsp. laumondii TTO1, a species which also has sep gene homologues.
Travis R. Glare - One of the best experts on this subject based on the ideXlab platform.
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Cloning Serratia entomophila Antifeeding Genes—a Putative Defective Prophage Active against the Grass Grub Costelytra zealandica
Journal of bacteriology, 2004Co-Authors: Mark R. H. Hurst, Travis R. Glare, Trevor A. JacksonAbstract:Serratia entomophila and Serratia proteamaculans (Enterobacteriaceae) cause Amber Disease in the grass grub Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. Larval Disease symptoms include cessation of feeding, clearance of the gut, Amber coloration, and eventual death. A 155-kb plasmid, pADAP, carries the genes sepA, sepB, and sepC, which are essential for production of Amber Disease symptoms. Transposon insertions in any of the sep genes in pADAP abolish gut clearance but not cessation of feeding, indicating the presence of an antifeeding gene(s) elsewhere on pADAP. Based on deletion analysis of pADAP and subsequent sequence data, a 47-kb clone was constructed, which when placed in either an Escherichia coli or a Serratia background exerted strong antifeeding activity and often led to rapid death of the infected grass grub larvae. Sequence data show that the antifeeding component is part of a large gene cluster that may form a defective prophage and that six potential members of this prophage are present in Photorhabdus luminescens subsp. laumondii TTO1, a species which also has sep gene homologues.
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cloning serratia entomophila antifeeding genes a putative defective prophage active against the grass grub costelytra zealandica
Journal of Bacteriology, 2004Co-Authors: Mark R. H. Hurst, Travis R. Glare, Trevor A. JacksonAbstract:Serratia entomophila and Serratia proteamaculans (Enterobacteriaceae) cause Amber Disease in the grass grub Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. Larval Disease symptoms include cessation of feeding, clearance of the gut, Amber coloration, and eventual death. A 155-kb plasmid, pADAP, carries the genes sepA, sepB, and sepC, which are essential for production of Amber Disease symptoms. Transposon insertions in any of the sep genes in pADAP abolish gut clearance but not cessation of feeding, indicating the presence of an antifeeding gene(s) elsewhere on pADAP. Based on deletion analysis of pADAP and subsequent sequence data, a 47-kb clone was constructed, which when placed in either an Escherichia coli or a Serratia background exerted strong antifeeding activity and often led to rapid death of the infected grass grub larvae. Sequence data show that the antifeeding component is part of a large gene cluster that may form a defective prophage and that six potential members of this prophage are present in Photorhabdus luminescens subsp. laumondii TTO1, a species which also has sep gene homologues.
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peripheral sequences of the serratia entomophila padap virulence associated region
Plasmid, 2003Co-Authors: Mark R. H. Hurst, Maureen Ocallaghan, Travis R. GlareAbstract:Abstract Some strains of the Enterobacteriaceae Serratia entomophila and Serratia proteamaculans cause Amber Disease in the grass grub, Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. The genes responsible for this Disease reside on a large, 155-kb plasmid designated Amber Disease-associated plasmid (pADAP). Herein, we report the DNA sequencing of approximately 50 kb upstream and 10 kb downstream of the virulence-encoding region. Based on similarity with proteins in the current databases, and potential ribosome-binding sites, 63 potential ORFs were determined. Eleven of these ORFs belong to a type IV pilus cluster ( pilL-V ) and a further eight have similarities to the translated products of the plasmid transfer traH-N genes of the plasmid R64. In addition, a degenerate 785-nt direct repeat flanks a 44.7-kb region with the potential to encode three Bacillus subtilis Yee-type proteins, a fimbrial gene cluster, the sep virulence-associated genes and several remnant IS elements.
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Restriction map of the Serratia entomophila plasmid pADAP carrying virulence factors for Costelytra zealandica
Plasmid, 2002Co-Authors: Mark R. H. Hurst, Travis R. GlareAbstract:Some strains of the Enterobacteriaceae Serratia entomophila and S. proteamaculans cause Amber Disease in the grass grub Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. The virulence determinants of the Disease reside on a large plasmid designated pADAP (Amber Disease-associated plasmid). A BamHI, EcoRI, and HindIII restriction cleavage map of pADAP was constructed by means of cloning restriction fragments. Each fragment was mapped, and neighboring fragments of mapped clones were systematically isolated from libraries using DNA probes constructed from previously cloned fragments. Through the use of sniff sequencing from the distal ends of a number of pADAP subclones the location of putative IS elements and genes involved in replication and conjugation were identified and assigned on the map. The location of the Amber Disease virulence-associated region was also mapped. The final map of pADAP spans 155 kb, 40 kb larger than the previous estimate.
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Plasmidlocated pathogenicity determinants of Serratia entomophila, the causal agent of Amber Disease of grass grub, show similarity to the insecticidal toxins of Photorhabdus luminescens
2000Co-Authors: Mark R. H. Hurst, Travis R. Glare, Trevor A. Jackson, Clive W. RonsonAbstract:Serratia entomophila and Serratia proteamaculans cause Amber Disease in the grass grub Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. Larval Disease symptoms include cessation of feeding, clearance of the gut, Amber coloration, and eventual death. A 115-kb plasmid, pADAP, identified in S. entomophila is required for Disease causation and, when introduced into Escherichia coli, enables that organism to cause Amber Disease. A 23-kb fragment of pADAP that conferred Disease-causing ability on E. coli and a pADAP-cured strain of S. entomophila was isolated. Using insertion mutagenesis, the pathogenicity determinants were mapped to a 17-kb region of the clone. Sequence analysis of the 17-kb region showed that the predicted products of three of the open reading frames (sepA, sepB, and sepC) showed significant sequence similarity to components of the insecticidal toxin produced by the bacterium Photorhabdus luminescens. Transposon insertions in sepA, sepB, orsepC completely abolished both gut clearance and cessation of feeding on the 23-kb clone; when recombined back into pADAP, they abolished gut clearance but not cessation of feeding. These results suggest that SepA, SepB, and SepC together are sufficient for Amber Disease causation by S. entomophila and that another locus also able to exert a cessation-of-feeding effect is encoded elsewhere on pADAP
Maureen Ocallaghan - One of the best experts on this subject based on the ideXlab platform.
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nucleotide sequence of the serratia entomophila plasmid padap and the serratia proteamaculans pu143 plasmid virulence associated region
Plasmid, 2011Co-Authors: Mark R. H. Hurst, Anette S Becher, Maureen OcallaghanAbstract:Some strains of Serratia entomophila and S. proteamaculans cause Amber Disease of the New Zealand grass grub Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. The Disease determinants of S. entomophila, are encoded on a 153,404-bp plasmid, termed pADAP for Amber Disease associated plasmid. The S. proteamaculans strain 143 (Sp143) exhibits an unusual pathotype, where only 60–70% of C. zealandica larvae infected with the bacterium succumb to Disease. DNA sequence analysis of the Sp143 pU143 virulence associated region identified high DNA similarity to the pADAP sep virulence associated region, with DNA sequence variation in the sepA gene and the variable region of the sepC component. No pADAP anti-feeding prophage orthologue was detected in the Sp143 genome. The region of pADAP replication was cloned and found to replicate in S. entomophila but not in Escherichia coli. DNA sequence analysis of the plasmid pSG348 repA gene from the French isolate of Serratia grimesii, identified 93% DNA identity to the pADAP repA gene. A comparison of the pU143 virulence associated region with the completed pADAP nucleotide sequence is given.
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establishment of serratia entomophila after application of a new formulation for grass grub control
New Zealand Plant Protection, 2004Co-Authors: R. J. Townsend, Trevor A. Jackson, Maureen Ocallaghan, C. M. Ferguson, J. R. Proffitt, M. W. A. Slay, J. Swaminathan, S. Day, E. M. Gerard, V. W. JohnsonAbstract:The bacterium Serratia entomophila is a naturally occurring pathogen causing Amber Disease of the New Zealand grass grub (Costelytra zealandica). A novel granular formulation of S. entomophila, Bioshield™, was applied to 18 pasture sites in a large-scale programme to demonstrate efficacy against grass grub. No significant difficulties were encountered in application of the granules through conventional machinery. There were high populations of the applied bacteria in soil within the first week of application, and within 6 weeks of application there was an average of 3 x 10 4 viable S. entomophila, of the applied strain, per gram of soil. This resulted in a significant (P<0.05) 20% increase in the incidence of Amber Disease in the treated grass grub populations compared to untreated populations. Successful establishment of the bacteria in the soil and target population following Bioshield™ granule application was demonstrated on a wide range of sites under various farming conditions.
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peripheral sequences of the serratia entomophila padap virulence associated region
Plasmid, 2003Co-Authors: Mark R. H. Hurst, Maureen Ocallaghan, Travis R. GlareAbstract:Abstract Some strains of the Enterobacteriaceae Serratia entomophila and Serratia proteamaculans cause Amber Disease in the grass grub, Costelytra zealandica (Coleoptera: Scarabaeidae), an important pasture pest in New Zealand. The genes responsible for this Disease reside on a large, 155-kb plasmid designated Amber Disease-associated plasmid (pADAP). Herein, we report the DNA sequencing of approximately 50 kb upstream and 10 kb downstream of the virulence-encoding region. Based on similarity with proteins in the current databases, and potential ribosome-binding sites, 63 potential ORFs were determined. Eleven of these ORFs belong to a type IV pilus cluster ( pilL-V ) and a further eight have similarities to the translated products of the plasmid transfer traH-N genes of the plasmid R64. In addition, a degenerate 785-nt direct repeat flanks a 44.7-kb region with the potential to encode three Bacillus subtilis Yee-type proteins, a fimbrial gene cluster, the sep virulence-associated genes and several remnant IS elements.
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isolation and enumeration of serratia entomophila a bacterial pathogen of the new zealand grass grub costelytra zealandica
Journal of Applied Microbiology, 1993Co-Authors: Maureen Ocallaghan, T. A. JacksonAbstract:Several agar media were tested for their use in a selective isolation and identification scheme for Serratia entomophila, a bacterium causing Amber Disease of the New Zealand grass grub, Costelytra zealandica (White). Soil dilutions were plated on caprylate thallous agar (CTA), selective for Serratia spp. Most strains of Ser. entomophila grew well on CTA; the mean efficiency of colony formation on CTA was 94 ± 3% of that on a non-selective medium. The identity of colonies growing on CTA was determined on the basis of their growth reactions on DNase-toluidine blue agar, adonitol agar and itaconate agar. Serratia entomophila could be distinguished from other Serratia spp. found in New Zealand soils, in particular Ser. proteamaculans, another causal agent of Amber Disease of grass grub. The identification scheme allowed the selective recovery of Ser. entomophila from field soils containing a diverse microflora.
Tony J. Sadler - One of the best experts on this subject based on the ideXlab platform.
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Association of a Large Plasmid with Amber Disease of the New Zealand Grass Grub, Costelytra zealandica, Caused by Serratia entomophila and Serratia proteamaculans
Journal of Invertebrate Pathology, 1993Co-Authors: Travis R. Glare, Geoffrey E. Corbett, Tony J. SadlerAbstract:Abstract Amber Disease, a chronic Disease of Costelytra zealandica (Coleoptera: Scarabaeidae) larvae, is caused by some isolates of the bacteria, Serratia entomophila and Serratia proteamaculans (Enterobacteriaceae). A large plasmid was visualized in some isolates of these two Serratia species. Further investigation showed that 18 of 19 pathogenic isolates of Serratia spp. were found to have a megaplasmid, estimated to be 105 kb. The one virulent isolate lacking a 105-kb plasmid had two smaller plasmids. The 105-kd plasmid was present in only 1 of 22 naturally occurring, nonpathogenic isolates examined. Plasmid DNA isolated from pathogenic isolates of each species showed identical restriction patterns. Heat-treated derivatives of pathogenic S. entomophila and S. proteamaculans isolates, which lost Disease-causing ability, also lost the 105-kb plasmid. Among isolates of 7 other species of Serratia, single isolates of Serratia grimesii and Serratia ficaria were found to have a similarly sized plasmid, but caused no Disease symptoms. The implications of the association between the plasmid and Amber Disease are discussed.