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Burkholderia
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Danielle L. Peters, Jaclyn G. McCutcheon, Karlene H. Lynch, Jonathan J. Dennis
More recently, the species Burkholderia gladioli has also been detected as a causative agent of the most prevalent foodborne illnesses. Since 2003, B. gladioli has been divided into four pathovars: gladioli, alliicola, agaricicola, and cocovenenans.9 The first three pathovars are primarily plant pathogens.10–12 However, in addition to being phytopathogenic, members of these pathovars can also infect immunocompromised patients with chronic granulomatous disease (CGD), cystic fibrosis (CF), and acquired immunodeficiency syndrome (AIDS).13–16 The taxonomic description of B. gladioli pvs. gladioli, alliicola, and agaricicola indicates that they do not produce toxins that are harmful to humans, although some strains have since been shown to synthesize toxoflavin.13,16 The fourth pathovar, B. gladioli pv. cocovenenans, is genetically similar to the first three, but distinct with regard to both its epidemiology and pathogenicity. Whereas other Burkholderia species can be isolated from food and water supplies, including B. pseudomallei, B. mallei, and members of the Bcc, B. gladioli pv. cocovenenans is the only species of the Burkholderia genus that is primarily characterized as a foodborne pathogen. B. gladioli pv. cocovenenans does not cause disease directly, but instead causes illness and death through the production of toxins that contaminate foods and beverages.
Escherichia coli
Published in Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward, Case Studies in Infectious Disease, 2010
Peter M. Lydyard, Michael F. Cole, John Holton, William L. Irving, Nino Porakishvili, Pradhib Venkatesan, Katherine N. Ward
Not all E. coli strains cause UTI and, in fact, E. coli (mainly of the K12 strain) is part of the normal flora of the intestine (i.e. a commensal) that normally does not cause any problems. However, different strains (pathovars) carry different virulence characteristics and are associated with different clinical outcomes (Table 1).
Burkholderia
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
Danielle L. Peters, Fatima Kamal, Jonathan J. Dennis
The genus Burkholderia covers a diverse group of Gram-negative β-proteobacteria. Although currently at least 60 species and proposed species exist in the genus Burkholderia, very few have been studied extensively. Much of the research to date has focused on the bacteria of the Burkholderia cepacia complex (Bcc), Burkholderia mallei, Burkholderia pseudomallei, and more recently, Burkholderia gladioli. The bacteria of the Bcc are pathogens that typically cause serious infections in plants, animals, and humans.1–3 However, they can also be beneficial in the environment as they fix nitrogen symbiotically for plants, produce antibiotics and antifungals, and have the capacity to degrade organic and xenobiotic compounds.4–6B. mallei causes “glanders,” a rare condition usually associated with horses, but that can also affect humans, whereas B. pseudomallei, endemic in Southeast Asia, causes “melioidosis,” a serious disease in humans with a wide variety of symptoms.7 The species B. gladioli has been divided into four pathovars: gladioli, alliicola, agaricicola, and cocovenenans.8 The first three B. gladioli pathovars listed are primarily plant pathogens,9–11 but members of these pathovars can occasionally also infect immunocompromised patients with chronic granulomatous disease (CGD), cystic fibrosis (CF), or acquired immune deficiency syndrome (AIDS).8,12,13 The taxonomic description of B. gladioli pvs. gladioli, alliicola, and agaricicola, published in 2003, suggests that they do not produce toxins that are harmful to humans, although some strains have since been shown to synthesize toxoflavin.8,14 The fourth B. gladioli pathovar, B. gladioli pv. cocovenenans, is distinct from the other pathovars with regards to its epidemiology and pathogenicity. Although the other Burkholderia species can be found as contaminants in food and water supplies (including the Bcc, B. mallei, and B. pseudomallei), B. gladioli pv. cocovenenans is the only bacterium of the Burkholderia genus that is traditionally characterized as a foodborne pathogen. Strains of B. gladioli pv. cocovenenans do not cause disease directly, but instead produce toxins that contaminate foods before ingestion by humans, similar to Clostridium botulinum. The laboratory infection models used to test Burkholderia pathogenicity and virulence are generally useful across the genera, whereas specific models have been devised to measure B. gladioli toxin activity. This chapter will briefly present the literature regarding the presence of B. mallei, B. pseudomallei, the Bcc, and B. gladioli in food and water supplies, and subsequently review the laboratory infection models that have been developed for each group of Burkholderia pathogenic bacteria.
Bacterial imbalance and gut pathologies: Association and contribution of E. coli in inflammatory bowel disease
Published in Critical Reviews in Clinical Laboratory Sciences, 2019
Shahanavaj Khan, Ahamad Imran, Abdul Malik, Anis Ahmad Chaudhary, Abdur Rub, Arif Tasleem Jan, Jakeera Begum Syed, Christian Rolfo
This pathovar differs from commensal gut E. coli strains due to its ability to adhere to and invade intestinal epithelium cells and replicate intracellularly in macrophages without stimulating interferon-γ (INF-γ) secretion or cell death [110]. Specific genes are needed for E. coli to adhere to and invade intestinal epithelium cells during replication in macrophages [111]. Macrophages provide the first line of defense by engulfing and killing invading pathogens. While the majority of bacteria can be effectively engulfed and removed by host macrophages, various pathogenic bacteria have evolved different strategies for phagosomal maturation [112]. For example, AIEC bacteria have the potential to replicate and survive in host macrophages [86,111]; high level of tumor necrosis factor-α (TNF, tumor necrosis factor) was observed in macrophages infected with AIEC [111]. The autophagy genes, ATG16L1, IRGM, and NOD2, are associated with identification and removal of intracellular bacteria. These genes are susceptible to mutations and are potentially involved in ileal CD. The AIEC pathotype with FimH (type 1 pilus adhesin) protein has high adhesion and invasive potential [111,113]. It has been observed that FimH proteins are able to bind to TLR4 to generate inflammatory responses [114]. This pathovar has specific binding affinity for carcinoembryonic antigen related cell adhesion molecule 6 (CEACAM6); altered CEACAM6 expression has been identified in ileal mucosa of CD [115,116]. In CD, CEACAM6 acts as a strong receptor for AIEC strains that colonize ileal mucosa [115].
Molecules involved in motility regulation in Escherichia coli cells: a review
Published in Biofouling, 2020
Fazlurrahman Khan, Nazia Tabassum, Dung Thuy Nguyen Pham, Sandra Folarin Oloketuyi, Young-Mog Kim
The presence of different E. coli pathovars and a diverse range of human and animal disease-causing properties necessitates efforts to study the underlying infection mechanisms (Dozois and Curtiss 1999; Croxen and Finlay 2010). Each pathovar and isolate of E. coli was shown to use a specific mechanism of infection (Kaper et al. 2004; Croxen and Finlay 2010; Connolly et al. 2019). Infection is in general achieved through initial adhesion to the host cells with the help of pili, fimbriae, and type III secretion system (T3SS) (Connolly JP et al. 2015). In addition to adhesion, the production of several other virulence factors is also responsible for causing diseases (Emody et al. 2003; Luthje and Brauner 2014; Connolly et al. 2015). Moreover, beyond pili and fimbriae, flagella facilitate adherence and biofilm formation (Wood et al. 2006; Haiko and Westerlund-Wikstrom 2013). Flagella also play a crucial role in chemotaxis towards environmental cues (Anderson et al. 2010). Here, the attractants from the biotic or abiotic surfaces trigger intracellular signaling mechanisms for flagella-mediated motility of the bacterial cells (Rossi, Paroni, et al. 2018). Flagella formation is inhibited throughout biofilm formation, and the cells within the biofilm thus become non-motile (Ryjenkov et al. 2006) (Figure 2C). Several studies have provided evidence regarding the role of flagella in motility of E. coli cells in the early stages of biofilm formation (Soutourina and Bertin 2003; Lehti et al. 2012; Friedlander et al. 2015). Hence, inhibiting the motility of E. coli is considered as a promising approach to minimizing biofilm formation and thereby development of infections.
A polymicrobial view of disease potential in Crohn's-associated adherent-invasive E. coli
Published in Gut Microbes, 2018
Wael Elhenawy, Alexander Oberc, Brian K. Coombes
E. coli is a diverse bacterial species whose members range from seemingly innocuous commensal strains to quite dangerous human pathogens. Pathovar designations are used to classify E. coli into groups with unique molecular mechanisms that govern their pathogenic behavior.26 The genetic determinants that help define E. coli pathovars (including serotype, toxins, and virulence factors) represent the basic tenets for their identification and facilitate the tracking of their evolutionary history.27,28 While much is known about the evolution of many E. coli pathotypes, the origin of the AIEC group is less clear. One key challenge in defining the AIEC pathovar is that the genetic factors conferring the adherent-invasive phenotype are not fully defined. Consequently, the identification of AIEC is done based on a series of in vitro phenotype assays that are laborious, time-consuming, and somewhat non-standardized. Also, virulence determinants that define other E. coli pathovars at the genetic level (i.e. Shiga toxin, type III secretion systems) are not found in AIEC.17 While this fact can be used as exclusion criteria when attempting to classify isolates of E. coli from patients, a molecular genetic signature that distinguishes the AIEC pathovar remains elusive. In a recent study, comparative whole-genome analysis of 14 AIEC strains identified a potential subgroup within the B2 phylotype that appeared more similar due to three genetic insertions that differentiated them from commensal E. coli.29 A separate study by a different group did not identify a readily distinguishable genomic signature among 11 different B2 phylotype AIEC strains although these strains were from a different geographic locale.22 As shown in different genomic studies, AIEC appear to be most closely related to extraintestinal E. coli strains such as UPEC, APEC, and ExPEC, which are also among the B2 clade.17,29,30 Furthermore, many virulence factors were found to be shared between AIEC and UPEC, including genes that are required for iron acquisition and transport.17 Together, these findings suggest that AIEC do not arise by parallel evolution and clonal expansion as described for the notorious O157:H7 enterohemorrhagic E. coli.31