Bacteria Causing Gastrointestinal Infections
K. Balamurugan, U. Prithika in Pocket Guide to Bacterial Infections, 2019
Most of these illness are self-limiting lasting only for few days and do not require antibiotics. Only severe and complicated cases require antibiotics, and in fact in some cases, antibiotics might even be harmful as with EHEC. Bacteria developing resistance toward antibiotics makes it mandatory to know the sensitivity pattern before selecting an antibiotic. This makes the isolation of organism even more important. As mentioned before, there has also been a changing trend of bacteria with falling incidence of well-known older infections (i.e., EHEC O157, Vibrio cholerae) and increasing incidence of other organisms (i.e., Campylobacter, Yersinia) with few maintaining a constant trend (i.e., Salmonella), and finally with lots of emerging organisms (i.e., Arcobacteria, Edwardsiella tarda, Plesiomonas shigelloides, Aeromonas hydrophila, Listeria monocytogenes, and Laribacter hongkongensis). This chapter discusses the general biology and transmission means of more common and emerging bacterial pathogens causing GI infection and describes various diagnostic and treatment methods. The order of the pathogens represents their contribution toward disease severity.
Ciprofloxacin
M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson in Kucers’ The Use of Antibiotics, 2017
The vast majority of enteric pathogens, including multiresistant isolates, are susceptible to ciprofloxacin, including Salmonella spp., Shigella spp., Campylobacter spp. (C. jejuni,. C. coli, C. fetus, C. cincaedi), Aeromonas spp. (A. hydrophila, A. sobria, A. caviae), Plesiomonas shigelloides, Vibrio cholerae, V. vulnificus and V. parahaemolyticus, Edwardsiella tarda, and Yersinia enterocolitica. However, resistance among Salmonella, Shigella, and Campylobacter species has increased significantly in some regions (Goodman et al., 1984; Fliegelman et al., 1985; Reinhardt and George, 1985; Mikhail et al., 1987; Bergan et al., 1988; Ling et al., 1988; Kain and Kelly, 1989; Burgos et al., 1990; Clark et al., 1990; Clark et al., 1991; Hyams et al., 1991; Pham et al., 1991; Sacks et al., 1991; Alós et al., 1992; John et al., 1992; Sjögren et al., 1992; Horiuchi et al., 1993; Newton and Kennedy, 1993; Preston et al., 1994; Vila et al., 1994; Tang et al., 2002; Thauvin-Eliopoulos and Eliopoulos, 2003; Lehtopolku et al., 2005; Biedenbach et al., 2006a; Lee et al., 2009; Vrints et al., 2009; Chiou et al., 2014; Cody et al., 2012; Folster et al., 2011; Garcia et al., 2014; Gaudreau et al., 2014; Gaudreau et al., 2015; Karki et al., 2013; Lee et al., 2009; Wong et al., 2014; Xia et al., 2011; see section 2b, Emerging resistance and cross-resistance).
Potential of Piper Germplasm Against Pathogenic Bacteria: Tropical Bay Islands in India
Megh R. Goyal, Durgesh Nandini Chauhan in Assessment of Medicinal Plants for Human Health, 2020
Studies with Edwardsiella tarda showed that Pipergenotypes could inhibit the growth of pathogen to some extent, whereas it remained lower than the inhibition observed for streptomycin (Table 5.5). In P. colubrinum-2, no inhibitory activity was seen, while P. colubrinum-1 showed inhibition zone at 100 µL. Contradictory reports are available for P. betle against the pathogen as some reports suggested its antibacterial activity,2,21 while poor response was observed in other,27 These variations could be attributed to the variation in the genotypes used and the strains/virulence of the pathogens employed.
The role of chitosan on oral delivery of peptide-loaded nanoparticle formulation
Published in Journal of Drug Targeting, 2018
Chun Y. Wong, Hani Al-Salami, Crispin R. Dass
Edwardsiella tarda can infect fish species, such as Japanese flounder, which causes emphysematous putrefactive disease, enteric septicaemia, gangrene and red disease [100]. The recombinant outer membrane protein A (rOmpA) of E. tarda was encapsulated in chitosan-based nanoparticles for oral vaccination of an endangered fish species called Labeo fimbriatus [101]. When compared to inactivated whole cell E. tarda vaccine, the rOmpA-loaded nanoparticles in oral vaccine produced higher level of antibodies, slower antigen release and superior protection against the pathogen. Therefore, oral vaccine can potentially be an effective immunisation strategy and increase the population of this fish species. Nevertheless, future studies should optimise the encapsulation efficiency.
Antibacterial activity of essential oils for combating colistin-resistant bacteria
Published in Expert Review of Anti-infective Therapy, 2022
Abdullah M. Foda, Mohamed H. Kalaba, Gamal M. El-Sherbiny, Saad A. Moghannem, Esmail M. El-Fakharany
The results obtained from the antibiotics susceptibility test of the five bacterial isolates referred to as these isolates are considered to be multidrug-resistant (MDR) bacteria, except E. coli AB-7. According to (CLSI) [28], the bacterial strain resistant to one antibiotic of three or more antibiotic classes is considered to be multidrug-resistant (MDR). Many studies have stated that there are various genera of Gram-negative bacteria that have acquired or natural resistance to colistin, such as Pseudomonas aeruginosa, Acinetobacter baumannii, Klebsiella pneumoniae, Escherichia coli, Proteus spp., Morganella morganii, Serratia spp., Providencia spp., Edwardsiella tarda, and Burkholderia cepacia. Most of the above-mentioned resistant bacteria have several mechanisms to defend themselves against polymyxins, such as the alteration of lipopolysaccharide (LPS) of the cell envelope, modifications of lipid A with phosphoethanolamine and 4-amino-4-deoxy-L-arabinose, furthermore, the use of efflux pumps, the development of capsules and overexpression of the outer membrane protein OprH, which are all efficiently controlled at the molecular level. All these strategies are thought to be responsible for the acquired and intrinsic resistance of polymyxins in these bacteria [30–33]. Gram-negative bacteria are resistant to colistin through intrinsic, adaptation, or mutation, in addition to horizontally acquired resistance via the mcr-1 gene and its variants [7].
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