Food-related factors influencing phage efficacy in reducing Campylobacter jejuni counts.

Distribution and characteristics of Campylobacter spp. in turkeys at slaughter.

Prevalence, antimicrobial resistance and virulence genes of Campylobacter isolated from retail duck meat in Southern China.

Colorectal cancer (CRC) remains a significant global health burden, with growing evidence highlighting microbial contributions to its pathogenesis. Certain genotoxigenic bacteria, such as Escherichia coli, Campylobacter jejuni, and Helicobacter pylori, produce virulence factors that induce DNA damage, genomic instability, and chronic inflammation—key features of carcinogenesis. At the same time, viruses such as JC polyomavirus (JCPyV), considered potentially oncogenic, and established oncogenic viruses like Epstein–Barr virus (EBV) and human papillomavirus (HPV) have been detected in colorectal tissues and are linked to cell cycle regulation, apoptosis, and DNA repair through their viral proteins. Intriguingly, recent findings suggest that bacterial genotoxins may promote the reactivation or transcriptional activity of persistent viruses such as JCPyV and EBV, possibly through DNA damage-induced stress and activation of NF-κB- or ATM-dependent signaling pathways. Despite these advances, interactions between oncogenic viruses and bacteria within the colon microbiome remain underexplored. This review integrates current evidence and provides future perspectives for addressing potential genotoxic collaboration between bacteria and viruses that could contribute to colorectal tumorigenesis. Elucidating these interactions could reveal novel biomarkers and therapeutic targets for the prevention and treatment of CRC.

Campylobacter is a foodborne pathogen that poses a serious threat to food safety and public health. Due to the limited data on the prevalence and antimicrobial resistance of Campylobacter across different retail meat sales modes in Southern China, this study primarily focuses on three sales modes of fresh, refrigerated, and frozen meat in Southern China. A total of 500 samples were collected from five cities in Guangdong Province between March and December 2021, with an overall Campylobacter detection rate of 20.8%, including only Campylobacter jejuni (53.8%) and Campylobacter coli (46.2%). The prevalence in fresh meat was significantly higher than in refrigerated and frozen meat and higher in butcher stalls than in supermarkets, with both chicken and pork showing a high prevalence. High resistance rates were also observed for ampicillin (95.2%), sulfamethoxazole (94.2%), and erythromycin (ERY; 90.4%), with 99.0% of isolates being multidrug resistant. The resistance of refrigerated and frozen meat was higher than that of fresh meat. This could be due to cold stress favoring the survival of resistant strains under selective pressure. The ERY resistance mechanisms were mainly mediated by the erm(B) gene, 23S rRNA mutations, and L22 ribosomal proteins. Multilocus sequence typing analysis indicated ST-828 clonal complex (CC828) as the most prevalent among ERY-resistant strains. This study reveals the prevalence patterns and high drug resistance levels of Campylobacter in retail meat in Southern China, providing a scientific basis for formulating targeted prevention and control measures for different sales modes.

Virulence and Immune Response of Campylobacter Jejuni Strains in Chicken Embryo Model.

Campylobacter jejuni (CJ), a major cause of bacterial gastroenteritis, employs exosomes to disseminate virulence factors and disrupt host immune homeostasis. This study investigated the therapeutic potential of Arabic Gum (AZ) and Lactobacillus acidophilus (LA), individually and in combination, against CJ exosome-induced intestinal injury in rats, with emphasis on inflammasome-related signaling and microbiota modulation. Rats received AZ, LA, or both following CJ exosome exposure. Molecular analyses, histopathology, and microbiome sequencing were performed to elucidate mechanistic responses. CJ exosomes activated key virulence pathways and triggered pronounced inflammatory signaling characterized by alpha kinase 1 (ALPK1), Nuclear Factor Kappa B (NF-κB), and NOD-like Receptor Pyrin (NLRP) upregulation, accompanied by epithelial injury and dysbiosis. Treatment with AZ or LA alone attenuated inflammasome activation and partially restored immune and microbial balance. Notably, the combined treatment produced a synergistic effect, effectively suppressing ALPK1/NF-κB/NLRP signaling and reestablishing a more physiologic microbial community structure. These improvements were associated with reductions in pro-inflammatory cytokines and markers of tissue damage, as well as substantial recovery in intestinal, hepatic, and splenic architecture. Overall, AZ and LA significantly mitigated CJ exosome-mediated pathology, with the combined therapy demonstrating superior efficacy. The findings suggest that co-administration of AZ and LA may offer a promising dual-modal strategy to counteract CJ-induced inflammatory and microbial disturbances, potentially supporting future therapeutic approaches targeting exosome-mediated pathogenesis.

Introduction: Campylobacter jejuni is a bacteria that is one of the most common causes of bacterial foodborne illness worldwide. The bacteria is typically transmitted through consumption of undercooked poultry, contaminated water, or unpasteurized dairy products. In addition to gastrointestinal symptoms such as diarrhea, abdominal cramps or fever, C. jejuni has been associated with post-infection sequelae, including rare cases of myocarditis. Although uncommon, myocarditis can result in arrhythmias, heart failure or even death, requiring prompt medical attention. Methods: This review consists of the latest papers, including cases, systematic reviews and cohorts. The analysis focuses on summarizing the C. jejuni infection-related myocarditis in male patients, in particular determining the time of onset of gastrointestinal and cardiovascular symptoms, and the results of additional tests leading to the diagnosis of myocarditis. Results: Among the 46 reported male patients with Campylobacter jejuni-associated myocarditis or myopericarditis, left ventricular systolic dysfunction was documented in 17 cases (39.5%). The time interval between the onset of gastrointestinal symptoms and the onset of chest pain was available for 43 patients, with a mean delay of 3,84 days (median 3 days; range 0-14 days), indicating a short but clearly discernible latency between enteric infection and myocardial involvement. Overall, only one of the 46 patients (2.2%) died, whereas all others survived to hospital discharge, indicating a generally favourable short-term prognosis despite the relatively high proportion of cases with impaired ventricular function. Conclusions: Proper food handling, cooking poultry to appropriate temperatures, and good hygiene practices are essential for prevention of C. jejuni infections. Quick and precise diagnosis of myocarditis prevents severe complications of the disease.

Campylobacter jejuni, a major cause of bacterial gastroenteritis, is capable of surviving in diverse hosts, including free-living amoebae such as Acanthamoeba. However, the molecular mechanisms that facilitate its intracellular persistence and subsequent transfer remain poorly defined. Here, we hypothesize that C. jejuni employs a biphasic actin-remodelling strategy, mediated by the effector proteins CiaI and CiaD, to reposition and remodel host mitochondria, promoting mitochondrial aggregation and iron homoeostasis. Using dual proteomics, microscopy, biochemical assays, and defined genetic mutants, we show that actin polymerization and CiaI are critical for mitochondrial interaction. We found that CiaI binds nucleotides with cooperative kinetics, acting as a molecular switch, and is crucial for C. jejuni localization near mitochondria, while CiaD promotes actin polymerization and acanthopodia formation to facilitate uptake. We propose a two-phase model: early actin polymerization repositions mitochondria, followed by localized actin depolymerization and mitochondrial remodelling. Iron chelation promotes bacterial survival, suggesting that oxidative stress functions as a host defence. These findings highlight a sophisticated mechanism of intracellular adaptation by C. jejuni that may be relevant to pathogenesis and identify new potential targets for disrupting its environmental and clinical persistence.

Characterization of the role of gluconate dehydrogenase in Campylobacter jejuni stress survival and host pathogenesis using Galleria mellonella infection model.

Campylobacteriosis and salmonellosis are the leading bacterial zoonoses in Europe, with poultry meat being the primary source of human contamination. Although both Campylobacter and Salmonella bacteria can coexist asymptomatically in chickens, their reciprocal impact remains underexplored. An in vitro study showed that Campylobacter jejuni survival was positively affected by the presence of Salmonella, but no data are available on this interaction in the animal gut. In this study, an in vivo investigation was carried out to explore the dynamics between Campylobacter and Salmonella colonization in chickens. The results revealed that both Salmonella and Campylobacter maintained significantly higher levels of colonization in the ceca throughout the experiment when co-inoculated compared to when inoculated alone. Additionally, changes in the microbiota were associated with each pathogen inoculated alone, but the simultaneous presence of Campylobacter and Salmonella induced specific modulations that could possibly explain this phenomenon. Significant differences were found in the serum metabolome of the contaminated groups, and partial least squares discriminant analysis models enabled the discrimination of contaminated animals from controls using these metabolic signals. Furthermore, possible links between variations in the microbiota and variations in the metabolome were identified.IMPORTANCEThis study demonstrates a synergistic effect between Salmonella and Campylobacter jejuni in the gut during co-infection in chickens, leading to an increased presence of both pathogens, as well as unique microbiota and metabolome changes. These findings underscore the importance of considering co-infection in poultry control measures and highlight the complex interplay between pathogens, microbiota, and metabolism.

Miller-Fisher syndrome (MFS) is a rare Guillain-Barré variant defined by ophthalmoplegia, ataxia, and areflexia. Pediatric MFS is uncommon, and infectious triggers remain underrecognized. Human herpesvirus 6 (HHV-6) is neurotropic but rarely linked to immune-mediated neuropathies. In this paper, we describe a child with MFS associated with HHV-6 detected in cerebrospinal fluid (CSF) and review reported pediatric infections related to MFS. A 5-year-old girl presented with acute ophthalmoplegia, ataxia, and diminished reflexes. Neuroimaging, ophthalmologic tests, CSF analyses, and serologic andpolymerase chain reaction (PCR) assays were performed, including multiplex reverse transcription-PCR of cerebrospinal fluid using the BioFire® Meningitis/Encephalitis panel. A literature search was performed on Pubmed to identify pediatric (0-18 years) MFS cases with infectious triggers. Two reviewers independently screened and summarized the literature, and a PRISMA-style flow diagram was used to transparently report the study selection process. HHV-6 DNA was detected via CSF PCR twice, while tests for other pathogens were negative. Anti-GQ1b and related antibodies were negative or borderline. The patient received intravenous immunoglobulin and corticosteroids, with full recovery after one month. Among 20 published pediatric cases (1997-2021), Campylobacter jejuni was most frequent, followed by Mycoplasma pneumoniae and influenza viruses. Anti-GQ1b IgM positivity and favorable outcomes were commonly reported, including cases managed conservatively. This case raises the hypothesis that HHV-6 may represent a potential post-infectious association in pediatric MFS. The review findings indicate that pediatric MFS generally follows infection, responds well to immunotherapy, and has an excellent prognosis. Viral testing may be considered in selected, hypothesis-generating contexts in atypical or seronegative pediatric MFS presentations.

Pseudaminic acids (Pse) are a family of carbohydrates found within bacterial lipopolysaccharides, capsular polysaccharides and glycoproteins that are critical for the virulence of human pathogens. However, a dearth of effective tools for detecting and enriching Pse has restricted study to only the most abundant Pse-containing glycoconjugates. Here we devise a synthesis of α- and β-O-pseudaminylated glycopeptides to generate 'pan-specific' monoclonal antibodies (mAbs) that recognize α- and β-configured Pse with diverse N7 acyl groups, as well as its C8 epimer (8ePse), presented within glycans or directly linked to polypeptide backbones. Structural characterization reveals the molecular basis of Pse recognition across a range of diverse chemical contexts. Using these mAbs, we establish a glycoproteomic workflow to map the Pse glycome of Helicobacter pylori, Campylobacter jejuni and Acinetobacter baumannii strains. Finally, we demonstrate that the mAbs recognize diverse capsule types in multidrug-resistant Acinetobacter baumannii and enhance phagocytosis to eliminate infections in mice.

Genomic insights into Campylobacter jejuni from Norwegian broilers: high genetic diversity and limited persistence on farms.

Mucosal delivery (in ovo and oral) of chitosan nanoparticle-based subunit vaccine enhances resistance against Campylobacter jejuni colonization in broiler chickens.

Peroxyacetic acid treatment significantly reduced Campylobacter jejuni culturability but not viability on chicken breasts

Glycosyltransferases (GTs) catalyze the formation of new glycosidic bonds and thus are vital for synthesizing nature’s vast repertoire of glycans and glycoconjugates and for engineering glycan-related medicines and materials. However, obtaining detailed structural and functional insights for the >750,000 known GTs is limited by difficulties associated with their efficient recombinant expression. Members of the GT-C fold, in particular, pose the most significant expression challenges due to the integration and folding requirements of their multiple membrane-spanning regions. Here, we address this challenge by engineering water-soluble variants of an archetypal GT-C fold enzyme, namely the oligosaccharyltransferase PglB from Campylobacter jejuni (CjPglB), which possesses 13 hydrophobic transmembrane helices. To render CjPglB water-soluble, we leveraged two advanced protein engineering methods: one that is universal called SIMPLEx (solubilization of IMPs with high levels of expression) and the other that is custom tailored called WRAPs (water-soluble RFdiffused amphipathic proteins). Each approach was able to transform CjPglB into a water-soluble enzyme that could be readily expressed in the cytoplasm of Escherichia coli cells at yields in the 3–6 mg/L range. Importantly, solubilization was achieved without the need for detergents and with retention of catalytic function. Collectively, our findings demonstrate that both SIMPLEx and WRAPs are promising platforms for advancing the molecular characterization of even the most structurally complex GTs, while also enabling broader GT-mediated glycosylation capabilities within synthetic glycobiology applications.

Guillain–Barré syndrome (GBS) is the most common and most severe acute paralytic neuropathy. There are different variants of GBS with distinct clinical and pathological features. Most GBS cases are preceded by infection or other immune stimulation that induces an aberrant autoimmune response targeting peripheral nerves and their spinal roots. Molecular mimicry between microbial and nerve antigens is clearly a major driving force behind the development of the disorder, at least in the case of Campylobacter jejuni infection. Some patients have been developing GBS either following or concomitant with head trauma, neurosurgical procedures, and rarely following stroke. The exact mechanism is not well understood probably blood–brain barrier damage may play an essential role in triggering the autoimmune activation that leads to post-stroke GBS.

Campylobacter jejuni is an important foodborne pathogen. To prevent human infections, special attention should be paid to prevention. Recently, methods involving essential oils have been considered as a means of reducing the number of contaminants in and on foods. This review summarizes the results of studies in which essential oils (EOs) with anti-campylobacter effects were tested. The most widely studied EOs were clove (28%), oregano (24%), thyme (22%), rosemary (8%), lavender (7%), sage (7%), and tea tree (4%), with other EOs studied to a lesser extent. The anti-Campylobacter efficacies of these EOs were demonstrated in vitro using a broad repertoire of methods, such as minimal inhibitory and bactericidal concentrations, agar diffusion, time-kill assays, adhesion and biofilm inhibitory assays, two-dimensional polyacrylamide gel electrophoresis, quantitative reverse-transcription PCR, and liquid chromatography-mass spectrometry. Recent studies have also focused on the practical application of such EOs, with experiments performed on different food matrices, typically chicken, duck, and beef. The most frequent treatment methods were mixing, dipping, and short-time freezing, either in packed or unpacked forms, and storage at different temperatures (typically 4 °C), although experiments were also performed at 25 °C, 32 °C, and 42 °C using different EO concentrations. In summary, these experiments revealed the anti-Campylobacter effects of thyme, cinnamon, coriander, lime, oregano, chrysanthemum, and basil.

Host-derived microRNAs (miRNAs) are known to regulate bacterial gene expression and maintain gut homeostasis. However, how these miRNAs survive harsh gut conditions to remain functional is not fully understood. This study tested whether extracellular vesicles (EV) carry microRNAs in the gut and whether infection with the enteric pathogen Campylobacter jejuni alters the microRNA profile packaged in these vesicles. We utilized fecal samples from mice, either maintained germ-free (absence of microbiota) or, C13 (defined 13 bacterial consortium), and C13 + C. jejuni to analyze the EV-derived miRNA pattern across the groups. Our results revealed distinct sets of miRNAs in each group and suggested possible interactions between these miRNAs and gene transcripts from both the host and bacteria. These findings provide new insights into how C. jejuni infection may change communication between the host and its microbiome, potentially affecting gut health and disease.