Susceptibility of suspended and surface-attached Salmonella enteritidis to biocides and elevated temperatures

Dhir, Vinod K.; Dodd, Christine E. R.

doi:10.1128/aem.61.5.1731-1738.1995

Cited by 79 publications

(25 citation statements)

References 47 publications

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“…Salmonella aggregates in food would also result in under estimation of bacterial load if standard cell counting procedures did not disperse the cell aggregates. Further studies will be needed to establish whether these thick Salmonella bio¢lms are resistant to sanitizers and other antimicrobial agents, as is often observed with various bio¢lms [4,6,7,9]. If so, knowledge of the Salmonella surface components contributing to bio¢lm development and resistance will lead to the development of more effective sanitizers.…”

Section: Discussionmentioning

confidence: 99%

Thin aggregative fimbriae enhance Salmonella enteritidis biofilm formation

Austin¹

1998

FEMS Microbiology Letters

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Salmonella enteritidis enteropathogens produce a variety of potentially adherent fimbrial types including SEF14, SEF17, SEF18 and SEF21 (type I). In a simplified, pure culture, biofilm generating system the virulent isolate, S. enteritidis 3b, readily adhered to Teflon (polytetrafluoroethylene) and stainless steel forming thick cell aggregates. The inability of an isogenic SEF17-deficient mutant to form thick biofilms suggested a role for SEF17 in stabilizing cell-cell interactions during biofilm formation. Epifluorescent detection of SEF17 in biofilms confirmed the association of these fimbriae with aggregated cells but not with adherent mutants unable to produce SEF17. The reduced adherence observed with an isogenic SEF14/SEF21-deficient strain implicated the involvement of additional cell surface adherence factors, possibly including SEF21 (type I) fimbriae in the adherence of S. enteritidis to stainless steel or Teflon. The role of SEF17 fimbriae in biofilm formation and the contributions of SEF17 to the persistence of Salmonellae on surfaces and in food are discussed. z 1998 Published by Elsevier Science B.V.

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Section: Discussionmentioning

confidence: 99%

Thin aggregative fimbriae enhance Salmonella enteritidis biofilm formation

Austin¹

1998

FEMS Microbiology Letters

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“…PAO1 lecA::lux has a disrupted lecA gene and consequently produces no LecA protein (Winzer et al ., 2000). Biofilm formation was monitored using a polystyrene microtitre plate assay and on stainless steel coupons (Dhir and Dodd, 1995). The mean absorbance in the microtitre assay, which is indicative of the degree of cell attachment to the polystyrene surface, was increased for the PA-IL-overproducing strain PAO-P47 (132% of that observed with PAO1), whereas the absorbance for the PAO1 lecA::lux mutant was significantly lower (49%) than that of the PAO1 wild type ( Fig.…”

Section: Leca Influences Biofilm Surface Coverage On Polystyrene and mentioning

confidence: 99%

“…Biofilms were grown on stainless steel coupons (grade 316L) under conditions similar to those described by Dhir and Dodd (1995). Stainless steel coupons were placed in Petri dishes with 10 ml of 0.05% (v/v) nutrient broth, or 10 ml of 0.05% (v/v) nutrient broth containing either 0.2 mM IPTG or 0.2 or 0.8 mM NPG, 0.2 or 0.013 mM NPF.…”

Section: Biofilm Formation On Stainless Steel Coupons (Static Assay)mentioning

confidence: 99%

The galactophilic lectin, LecA, contributes to biofilm development in Pseudomonas aeruginosa

Diggle

Stacey

Dodd

et al. 2006

Environmental Microbiology

295

274

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LecA (PA-IL) is a cytotoxic lectin and adhesin produced by Pseudomonas aeruginosa which binds hydrophobic galactosides with high specificity and affinity. By using a lecA-egfp translation fusion and immunoblot analysis of the biofilm extracellular matrix, we show that lecA is expressed in biofilm-grown cells. In static biofilm assays on both polystyrene and stainless steel, biofilm depth and surface coverage was reduced by mutation of lecA and enhanced in the LecA-overproducing strain PAO-P47. Biofilm surface coverage by the parent strain, PAO-P47 but not the lecA mutant on steel coupons was also inhibited by growth in the presence of either isopropyl-beta-D-thiogalactoside (IPTG) or p-nitrophenyl-alpha-D-galactoside (NPG). Furthermore, mature wild-type biofilms formed in the absence of these hydrophobic galactosides could be dispersed by the addition of IPTG. In contrast, addition of p-nitrophenyl-alpha-L-fucose (NPF) which has a high affinity for the P. aeruginosa LecB (PA-IIL) lectin had no effect on biofilm formation or dispersal. Planktonic growth of P. aeruginosa PAO1 was unaffected by the presence of IPTG, NPG or NPF, nor was the strain able to utilize these sugars as carbon sources, suggesting that the observed effects on biofilm formation were due to the competitive inhibition of LecA-ligand binding. Similar results were also obtained for biofilms grown under dynamic flow conditions on steel coupons, suggesting that LecA contributes to P. aeruginosa biofilm architecture under different environmental conditions.

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“…Another explanation could be that Campylobacter spp. present in the crates were likely to be embedded in organic matter and therefore more protected than if they were freely suspended (Dhir and Dodd 1995).…”

Section: Contamination By Cratesmentioning

confidence: 99%

Transmission of Campylobacter spp. to chickens during transport to slaughter

Hansson

Ederoth

Andersson³

et al. 2005

J Appl Microbiol

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Aims: To determine the prevalence of Campylobacter-contaminated transport crates and to determine whether contaminated crates represent a risk for contamination of chickens during transport to slaughter. Methods and Results: Samples were collected from cleaned transport crates before they were dispatched to the farms. Chicken groups were sampled within 24 h before transport to slaughter and at the slaughterhouse. Campylobacter spp. were isolated from 69 of 122 (57%) sampled batches of transport crates. Twenty-six slaughter groups, negative at farm level, were transported in batches of crates from which Campylobacter spp. had been isolated. In 11 (42%) of these 26 slaughter groups, Campylobacter spp. were found in samples taken at slaughter. The corresponding figure for at-farm-negative slaughter groups transported in negative crates was four (15%) testing positive at slaughterhouse of 27 slaughter groups [relative risk (RR) ¼ 2AE9, 95% CI 1AE1-7AE3]. In four of 11 slaughter groups, genetic subtyping by pulsed-field gel electrophoresis was able to support the hypothesis of contamination from crates to chickens during transport to slaughter. Conclusions: Despite washing and disinfection, crates were frequently contaminated with Campylobacter and it could have contaminated chickens during transport to slaughter. Significance and Impact of the Study: Campylobacter-positive crates are a risk factor for chickens testing campylobacter-positive at slaughter.

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Susceptibility of suspended and surface-attached Salmonella enteritidis to biocides and elevated temperatures

Cited by 79 publications

References 47 publications

Thin aggregative fimbriae enhance Salmonella enteritidis biofilm formation

Thin aggregative fimbriae enhance Salmonella enteritidis biofilm formation

The galactophilic lectin, LecA, contributes to biofilm development in Pseudomonas aeruginosa

Transmission of Campylobacter spp. to chickens during transport to slaughter

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