Emergence and Molecular Epidemiology of Campylobacter jejuni ST-2993 Associated with a Large Outbreak of Guillain-Barré Syndrome in Peru

Quino, Willi; Caro-Castro, Junior; Mestanza, Orson; Hurtado, Verónica; Zamudio, María Luz; Cruz-Gonzales, Gloria; Gavilán, Ronnie G.

doi:10.1128/spectrum.01187-22

Cited by 9 publications

(9 citation statements)

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“…An association between Campylobacter jejuni enteritis and GBS helped establish the concept of molecular mimicry in GBS pathogenesis. C. jejuni expresses surface lipooligosaccharides that mimic human gangliosides present in peripheral nerve fibers 86 . Antibodies generated against the bacterial lipooligosaccharides cross‐react with gangliosides like GM1 and GD1a in peripheral nerves, due to shared oligosaccharide epitopes 87 .…”

Section: Gbsmentioning

confidence: 99%

“…C. jejuni expresses surface lipooligosaccharides that mimic human gangliosides present in peripheral nerve fibers. 86 Antibodies generated against the bacterial lipooligosaccharides cross‐react with gangliosides like GM1 and GD1a in peripheral nerves, due to shared oligosaccharide epitopes. 87 This mimicking of nerve gangliosides allows C. jejuni to induce potentially pathogenic anti‐ganglioside antibodies through molecular mimicry.…”

Section: Gbsmentioning

confidence: 99%

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Potential clinical implications of molecular mimicry‐induced autoimmunity

Suliman

2024

Immunity Inflam & Disease

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BackgroundMolecular mimicry is hypothesized to be a mechanism by which autoimmune diseases are triggered. It refers to sequence or structural homology between foreign antigens and self‐antigens, which can activate cross‐reactive lymphocytes that attack host tissues. Elucidating the role of molecular mimicry in human autoimmunity could have important clinical implications.ObjectiveTo review evidence for the role of molecular mimicry in major autoimmune diseases and discuss potential clinical implications.MethodsComprehensive literature review of clinical trials, observational studies, animal models, and immunology studies on molecular mimicry in multiple sclerosis, type 1 diabetes, rheumatoid arthritis, lupus, Guillain‐Barre syndrome, autoimmune myocarditis, and primary biliary cirrhosis published from 2000–2023.ResultsSubstantial indirect evidence supports molecular mimicry as a contributor to loss of self‐tolerance in several autoimmune conditions. Proposed microbial triggers include Epstein‐Barr virus, coxsackievirus, Campylobacter jejuni, and bacterial commensals. Key mechanisms involve cross‐reactive T cells and autoantibodies induced by epitope homology between microbial and self‐antigens. Perpetuation of autoimmunity involves epitope spreading, inflammatory mediators, and genetic factors.ConclusionsMolecular mimicry plausibly explains initial stages of autoimmune pathogenesis induced by infection or microbiota disturbances. Understanding mimicry antigens and pathways could enable improved prediction, monitoring, and antigen‐specific immunotherapy for autoimmune disorders. However, definitive proof of causation in humans remains limited. Further research should focus on establishing clinical evidence and utility.

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Section: Gbsmentioning

confidence: 99%

Section: Gbsmentioning

confidence: 99%

Potential clinical implications of molecular mimicry‐induced autoimmunity

Suliman

2024

Immunity Inflam & Disease

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“…Los departamentos con mayor número de casos fueron Lima, La Libertad, Lambayeque, Cajamarca, Piura, Junín, Callao y Cusco (11) . Ante ello, es necesario precisar que el brote de dengue tuvo un incremento marcado de casos hacia la semana 15 con un pico hacia la semana 20 que fue posteriormente en descenso, mientras que los casos de SGB se incrementaron entre la SE 23 y 27 (7) , donde se reportaron 96 casos, de los cuales el 77,1 % fueron procedentes de los departamentos de Lima (25 casos), La Libertad (15), Lambayeque (14), Piura (12) y Cajamarca (8) (11) . De este modo, estos datos revelan un pico de casos de SGB dos semanas después del pico de casos de dengue (Figura 1), lo cual hace suponer una asociación entre ambas entidades.…”

Section: Posible Vínculo De La Infección Por Dengue Y Zika Con El Aum...unclassified

“…El sustento de esta asociación; C. jejuni -SGB en el Perú, se remonta a reportes de 2019 en el que el país informó un brote de SGB sin precedentes, que afectó a varias regiones, con más de 900 casos notificados. A partir de las características epidemiológicas clínicas y el estudio de los agentes identificados, se concluyó que este brote se asoció con la presencia del genotipo C. jejuni ST2993 (11) y, para llegar a esta conclusión, se secuenciaron tan solo 21 genomas de C. jejuni pertenecientes al ST-2293, obtenidas entre 2019 y 2020 (14) .Este estudio proporcionó información importante sobre la epidemiología molecular de las cepas de C. jejuni asociadas con un brote de SGB en Perú. Sin embargo, es importante tener en cuenta que ningún estudio es completamente concluyente, ya que siempre existen limitaciones en términos de las muestras analizadas, el diseño del estudio y otros factores.…”

Section: Posible Vínculo De La Infección Por Dengue Y Zika Con El Aum...unclassified

El Síndrome de Guillain-Barré en Perú: ¿Dengue y Zika detrás del aumento de casos?

Aguilar-Gamboa

2023

Rev Exp Med

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In 2023, Peru experienced the largest dengue outbreak in its history, with over 197,000 confirmed cases. Between epidemiological weeks 23 and 27 of that year, there was a peak in cases of Guillain-Barré syndrome (GBS), just two weeks after the peak of dengue cases. There is previous evidence associating dengue with the development of GBS, suggestingthat the dengue virus may be responsible for many of the current cases. Additionally, there were 31 cases of Zika recorded in Peru in 2023, a neurotropic virus that has also been previously linked to GBS. While there has been speculation in some media about the current GBS outbreak being related to Campylobacter jejuni in chickens, there is no conclusive evidence supporting this claim. It is necessary to conduct in-depth investigations into the presence of dengue and Zika in samples from patients with GBS to understand the potential causal role of these viruses. Studying the relationship between these infectious agents and the development of GBS can enhance prevention and treatment strategies for future epidemiological threats.

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“…Despite the importance of Campylobacter as an emerging enteric pathogen, its prevalence in low and middle-income countries is widely unknown ( Platts-Mills and Kosek, 2014 ; Kaakoush et al., 2015 ; Collado et al., 2018 ; Levican et al., 2019 ; Collado, 2020 ). Recent reports in the Latin American region have shown a high prevalence of human campylobacteriosis ( Porte et al., 2023 ), including significant outbreaks causing long-term autoimmune sequelae such as GBS ( Ramos et al., 2021 ; Quino et al., 2022 ). The absence of widely globally distributed lineages in some areas of Latin American countries such as Peru ( Pascoe et al., 2020 ) emphasizes the need to gain a deeper insight into the molecular epidemiology and characteristics of the predominance of particular genotypes in the region.…”

Section: Introductionmentioning

confidence: 99%

Whole-genome sequencing reveals changes in genomic diversity and distinctive repertoires of T3SS and T6SS effector candidates in Chilean clinical Campylobacter strains

Katz,

Porte,

Weitzel

et al. 2023

Front. Cell. Infect. Microbiol.

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Campylobacter is the leading cause of bacterial gastroenteritis worldwide and an emerging and neglected pathogen in South America. This zoonotic pathogen colonizes the gastrointestinal tract of a wide range of mammals and birds, with poultry as the most important reservoir for human infections. Apart from its high morbidity rates, the emergence of resistant strains is of global concern. The aims of this work were to determine genetic diversity, presence of antimicrobial resistance determinants and virulence potential of Campylobacter spp. isolated from patients with acute gastrointestinal disease at ‘Clinica Alemana’, Santiago de Chile. The study considered the isolation of Campylobacter spp., from stool samples during a 20-month period (January 2020 to September 2021). We sequenced (NextSeq, Illumina) and performed an in-depth analysis of the genome sequences of 88 Campylobacter jejuni and 2 Campylobacter coli strains isolated from clinical samples in Chile. We identified a high genetic diversity among C. jejuni strains and the emergence of prevalent clonal complexes, which were not identified in our previous reports. While ~40% of strains harbored a mutation in the gyrA gene associated with fluoroquinolone resistance, no macrolide-resistance determinants were detected. Interestingly, gene clusters encoding virulence factors such as the T6SS or genes associated with long-term sequelae such as Guillain-Barré syndrome showed lineage-relatedness. In addition, our analysis revealed a high degree of variability regarding the presence of fT3SS and T6SS effector proteins in comparison to type strains 81-176, F38011, and NCTC 11168 and 488. Our study provides important insights into the molecular epidemiology of this emerging foodborne pathogen. In addition, the differences observed regarding the repertoire of fT3SS and T6SS effector proteins could have an impact on the pathogenic potential and transmissibility of these Latin American isolates, posing another challenge in characterizing the infection dynamics of this emergent and neglected bacterial pathogen.

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Emergence and Molecular Epidemiology of Campylobacter jejuni ST-2993 Associated with a Large Outbreak of Guillain-Barré Syndrome in Peru

Cited by 9 publications

References 46 publications

Potential clinical implications of molecular mimicry‐induced autoimmunity

Potential clinical implications of molecular mimicry‐induced autoimmunity

El Síndrome de Guillain-Barré en Perú: ¿Dengue y Zika detrás del aumento de casos?

Whole-genome sequencing reveals changes in genomic diversity and distinctive repertoires of T3SS and T6SS effector candidates in Chilean clinical Campylobacter strains

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