• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.7
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• pp.1041-1048
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• 2016

Biofilm cells and viable but non-culturable (VBNC) state may play a role in the survival of Campylobacter jejuni under unfavorable environmental conditions. The objective of this study was to investigate the behavior of C. jejuni biofilm cells and VBNC cells on smoked duck. The transfer of C. jejuni biofilm cells to smoked duck and its ability to resuscitate from biofilm and VBNC cells on smoked duck was investigated. Transfer experiments were conducted from C. jejuni biofilm cells to smoked duck after 5 min, 1 h, 3 h, and 24 h contact at room temperature, and the efficiency of transfer (EOT) was calculated. In addition, smoked duck was inoculated with C. jejuni biofilm and VBNC cells and then stored at 10, 24, 36, and $42^{\circ}C$ to examine the cells' ability to resuscitate on smoked ducks. The 5 min contact time between C. jejuni biofilm cells and smoked duck showed a higher EOT (0.92) than the 24 h contact time (EOT=0.08), and the EOT decreased as contact time increased. Furthermore, C. jejuni biofilm cells on smoked duck were not recovered at 10, 24, and $36^{\circ}C$, and C. jejuni VBNC cells were not resuscitated at $42^{\circ}C$. Although the resuscitation of C. jejuni biofilm and VBNC cells was not observed on smoked duck, microbial criteria of C. jejuni is needed in poultry and processed poultry products due to risk of its survival and low infectious dose.

• Asian-Australasian Journal of Animal Sciences
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• v.7 no.4
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• pp.505-507
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• 1994

A total of 526 domestic and experimental animals in Miyagi prefecture, Japan were investigated for fecal carriage of Campylobacter jejuni and Campylobacter coli. C. jejuni was detected in chickens (8.2%), dogs (6.3%), pigs (4.3%), cattle (1.8%) and hamsters (1.4%). C. coli was only detected from pigs (20.7%). Drug susceptibility test was performed on 5 strains of C. jejuni isolated from chickens and 13 strains of C. coli isolated from pigs to tylosin (TS), thianphenicol (TP), carbadox (CDX), chroltetracyclin (CTC), vancomycin (VCM), cefoperazone (CPZ), latamoxef (LMOX), GM were highly effective and CTC, CP and PL were moderately effective against both C. jejuni and C. coli. TS and TPH were moderately effective against C. jejuni; however, they were less effective to C. coli. One strain of C. jejuni against CTC considered to be drug resistant. The results suggest that C. jejuni and C. coli can be controlled by several drugs effectively, although a drug resistant strain exists.

• Journal of Microbiology and Biotechnology
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• v.27 no.11
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• pp.1942-1951
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• 2017

Campylobacter jejuni and Campylobacter coli are important foodborne pathogenic bacteria, particularly in poultry meat. In this study, the presence of extracellular DNase activity was investigated for biofilm-deficient Campylobacter strains versus biofilm-forming Campylobacter strains isolated from chickens, to understand the relationship between extracellular DNase activity and biofilm formation. A biofilm-forming reference strain, C. jejuni NCTC11168, was co-incubated with biofilm non-forming strains isolated from raw chickens or their supernatants. The biofilm non-forming strains or supernatants significantly prohibited the biofilm formation of C. jejuni NCTC11168. In addition, the strains degraded pre-formed biofilms of C. jejuni NCTC11168. Degradation of C. jejuni NCTC11168 biofilm was confirmed after treatment with the supernatant of the biofilm non-forming strain 2-1 by confocal laser scanning microscopy. Quantitative analysis of the biofilm matrix revealed reduction of extracellular DNA (16%) and proteins (8.7%) after treatment. Whereas the biofilm-forming strains C. jejuni Y23-5 and C. coli 34-3 isolated from raw chickens and the C. jejuni NCTC11168 reference strain showed no extracellular DNase activity against their own genomic DNA, most biofilm non-forming strains tested, including C. jejuni 2-1, C. coli 34-1, and C. jejuni 63-1, exhibited obvious extracellular DNase activities against their own or 11168 genomic DNA, except for one biofilm non-former, C. jejuni 22-1. Our results suggest that extracellular DNase activity is a common feature suppressing biofilm formation among biofilm non-forming C. jejuni or C. coli strains of chicken origin.

• Korean Journal of Microbiology
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• v.32 no.1
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• pp.47-52
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• 1994

The cells of Campylobacter jejuni heat-shocked at 48${\circ}C$ for 30 min synthesized the heat shock proteins of HSP90, HSP66 and HSP60. Those heat shock proteins were found to correspond to the heat shock proteins of HSP87, HSP66 (DnaK), and HSP58 (GroEL) of E. coli, respectively. By Southern blot analysis of the chromosomal DNAs of C. jejuni with groESL and dnaK genes of E. coli as DNA probes, the heat shock genes of C. jejuni which are homologous to the E. coli groESL and dnaK genes were found to exist in the chromosomal DNA. The genomic libraries of C. jejuni were constructed with the cosmid vector pWE15 and the groEL gene of C. jejuni were cloned in E. coli B178 groEL44 temperature senstive mutant. The hybrid plasmid (pLC1) was inserted with the DNA fragment (about 5.7kb in size) containing the groEL gene. E. coli groEL44 mutant cell transformed with the pLC1 could grow at 42${\circ}C$ by synthesizing the HSP60 of C. jejuni and regained the susceptibility to the ${\lambda}$ vir phage by expression of the groEL gene in the cloned cells. These indicated that the groEL products of C. jejuni had chaperon effects by synthesizing the heat shock proteins in the cloned cells of E. coli.

• Asian-Australasian Journal of Animal Sciences
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• v.32 no.2
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• pp.274-281
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• 2019

Objective: The objective of this study was to estimate the risk of Campylobacter jejuni (C. jejuni) infection from various jerky products in Korea. Methods: For the exposure assessment, the prevalence and predictive models of C. jejuni in the jerky and the temperature and time of the distribution and storage were investigated. In addition, the consumption amounts and frequencies of the products were also investigated. The data for C. jejuni for the prevalence, distribution temperature, distribution time, consumption amount, and consumption frequency were fitted with the @RISK fitting program to obtain appropriate probabilistic distributions. Subsequently, the dose-response models for Campylobacter were researched in the literature. Eventually, the distributions, predictive model, and dose-response model were used to make a simulation model with @RISK to estimate the risk of C. jejuni foodborne illness from the intake of jerky. Results: Among 275 jerky samples, there were no C. jejuni positive samples, and thus, the initial contamination level was statistically predicted with the RiskUniform distribution [RiskUniform (-2, 0.48)]. To describe the changes in the C. jejuni cell counts during distribution and storage, the developed predictive models with the Weibull model (primary model) and polynomial model (secondary model) were utilized. The appropriate probabilistic distribution was the BetaGeneral distribution, and it showed that the average jerky consumption was 51.83 g/d with a frequency of 0.61%. The developed simulation model from this data series and the dose-response model (Beta Poisson model) showed that the risk of C. jejuni foodborne illness per day per person from jerky consumption was $1.56{\times}10^{-12}$. Conclusion: This result suggests that the risk of C. jejuni in jerky could be considered low in Korea.

• Korean Journal of Microbiology
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• v.30 no.5
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• pp.377-382
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• 1992

The responses of C. jejuni to ethanol shock were studied for their survival. synthesis of ethanol shock proteins, and increased survival at higher concentration of ethanol upon prior treatments of ethanol. When C. jejuni were shocked with ethanol at 1. 3. and 5% for 60. 30 and 10 minutes, respectively. those cells synthesized the ethanol shock proteins of 90, 66, 60, 45, and 24 kd in molecular weight. When the C. ,jejuni shocked with 1 and 3% ethanol were exposed to 3 and 5% ethanol for 30 minutes. their survival rates were increased by $10^1$~$10^2$ as compared with those of the cells without ethanol-shock. In the same way. C. ,jejuni shocked with 5% ethanol for 10 minutes :.bowed about 102 times higher survival rates than the cells without ethanol-shock. This result suggests that C jejuni shocked with I-5% ethanol for 10-30 minutes synthesized five kinds of ethanol shock proteins. and that the shock proteins contributed to increase ethanol tolerance for their survival at the higher concentrations of ethanol.

• Korean Journal of Microbiology
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• v.29 no.1
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• pp.49-55
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• 1991

The heat shock responses of Campylobacter jejuni were studied by examination of their survival rates and synthesis of heat shocd proteins. When C. jejuni cells were treated at the sublethal temperatures of 48.deg.C for 30 minutes, most of the cells maintained their viabilities and synthesized the heat shock proteins of 90, 73, and 66 kD in molecular weight. By the method of two-dimensional electrophoresis, the heat shock proteins of C. jejuni were identified to be Hsp90, Hsp73, and Hsp66. During the heat shock at 48.deg.C, the heat shock proteins were induced from about 5 minutes after the heat shock treatment. Their synthesis was continued upto 30 minutes, but remarkably retarded after 50 minutes. When C. jejune cells were heat shocked at 51.deg.C for 30 minutes, the survival rates of the cells were decreased by about $10^{3}$ fold and synthesis of heat shock proteins and normal proteins was also generally retarded. The cells exposed to 55.deg.C for 30 minutes died off by more than $10^{5}$ cells and the new protein synthesis was not observed. But when C. jejuni cells were heat-shocked at the sublethal temperature of 48.deg.C for 15 to 20 minutes and then were exposed at the lethal temperature of 55.deg.C for 30 minutes, their viabilities were higher than those exposed at 55.deg.C for 30 minutes without pre-heat shock at 48.deg.C. Therefore, the heat shock proteins synthesized at the sublethal temperature of 48.deg.C in C. jejuni were thought to be responsible for thermotolerance. However, when C. jejuni cells heat-shocked at various ranges of sublethal and lethal temperatures were placed back to the optimum temperature of 42.deg.C, the multiplication patterns of the cells pretreated at different temperatures were not much different each other.

• Journal of Microbiology and Biotechnology
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• v.25 no.11
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• pp.1871-1879
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• 2015

The complex roles of flagella in the pathogenesis of Campylobacter jejuni, a major cause of worldwide foodborne diarrheal disease, are important. Compared with the wild-type, an insertional mutation of the flgA gene (cj0769c) demonstrated significant decrease in the biofilm formation of C. jejuni NCTC11168 on major food contact surfaces, such as polystyrene, stainless steel, and borosilicate glass. The flgA mutant was completely devoid of flagella and non-motile whereas the wild-type displayed the full-length flagella and motility. In addition, the biofilm formation of the wild-type was inversely dependent on the viscosity of the media. These results support that flagellar-mediated motility plays a significant role in the biofilm formation of C. jejuni NCTC11168. Moreover, our adhesion assay suggests that it plays an important role during biofilm maturation after initial attachment. Furthermore, C. jejuni NCTC11168 wild-type formed biofilm with a net-like structure of extracellular fiber-like material, but such a structure was significantly reduced in the biofilm of the flgA mutant. It supports that the extracellular fiber-like material may play a significant role in the biofilm formation of C. jejuni. This study demonstrated that flgA is essential for flagellar biosynthesis and motility, and plays a significant role in the biofilm formation of C. jejuni NCTC11168.

• Korean Journal of Microbiology
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• v.30 no.3
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• pp.232-238
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• 1992

Canz~~j~lohuc;tc.~jurn i werc studied for their heat shock responses at several elevated temperatures and their heat shock genes were detected by the technique of Southern hybridization. (.. ,jc\ulcorneruni sy~>thesized the major heat shock proteins of hsp90. hsphh. and hsphO at 48$^{\circ}$C . ant1 their w~u.ival rates were maintained as the same level at optimal temperature. '1-hc heat shock genes in chromosome of C ,jc:jutii werc determined to be homologous to the heat shock genes or E. t,oli. by showing strong signals in Southern hybridization analysis using clnaK and groESL- as DNA probe But the restriction sites for thc fragmcnts including heat shock genes were different betueen E. c,oli and C ,jtjuni.

• Journal of Microbiology and Biotechnology
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• v.27 no.9
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• pp.1609-1616
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• 2017

The complex roles of cell surface modification in the biofilm formation of Campylobacter jejuni, a major cause of worldwide foodborne diarrheal disease, are poorly understood. In a screen of mutants from random transposon mutagenesis, an insertional mutation in the eptC gene (cj0256) resulted in a significant decrease in C. jejuni NCTC11168 biofilm formation (<20%) on major food contact surfaces, such as polystyrene and borosilicate glass, when compared with wild-type cells (p < 0.05). In C. jejuni strain 81-176, the protein encoded by eptC modified cell surface structures, such as lipid A, the inner core of lipooligosaccharide, and the flagellar rod protein (FlgG), by attaching phosphoethanolamine. To assess the role of eptC in C. jejuni NCTC11168, adherence and motility tests were performed. In adhesion assays with glass surfaces, the eptC mutant exhibited a $0.77log\;CFU/cm^2$ decrease in adherence compared with wild-type cells during the initial 2 h of the assay (p < 0.05). These results support the hypothesis that the modification of cell surface structures by eptC affects the initial adherence in biofilm formation of C. jejuni NCTC11168. In motility tests, the eptC mutant demonstrated reduced motility when compared with wild-type cells, but wild-type cells with the transposon inserted in a gene irrelevant to biofilm formation (cj1111c) also exhibited decreased motility to a similar extent as the eptC mutant. This suggests that although eptC affects motility, it does not significantly affect biofilm formation. This study demonstrates that eptC is essential for initial adherence, and plays a significant role in the biofilm formation of C. jejuni NCTC11168.