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Cryptosporidium spp
Published in Peter D. Walzer, Robert M. Genta, Parasitic Infections in the Compromised Host, 2020
Difficulty in separating or identifying the roles of the different components of the neonatal calf diarrhea complex, along with the finding of asymptomatic Cryptosporidium sp. infections has led some to question the role of this coccidian as a primary pathogen (94). The controversy as to whether Cryptosporidium sp. is a true enteropathogen in the absence of other agents of enteric disease in calves has, to my satisfaction, been resolved. The typical clinical signs of diarrhea and malabsorption, and the characteristic lesions of villous blunting, atrophy, and fusion noted in naturally and experimentally infected animals also occur in gnotobiotic calves monoinfected with C. parvum (79). Heine et al. (79) suggested that malabsorption caused by villous atrophy resulting from accelerated loss of epithelium was the basis for Cryptosporidium-induced diarrhea in these calves. Similar findings also have been published for gnotobiotic pigs (95) and gnotobiotic lambs (96) that were reported to be moninfected with C. patvum. Thus, it appears that most of the C. parvum isolates studied to date are primary pathogens that cause diarrhea in calves. As with any primary enteropathogen, one should expect to find some animals infected with C. parvum that have no clinical signs of illness. The finding of large numbers of infected calves without diarrhea in a herd would suggest that different isolates of C. parvum may vary markedly in their virulence. Such differences in virulence have been suggested by others (1,94).
Gastrointestinal and liver infections
Published in Michael JG Farthing, Anne B Ballinger, Drug Therapy for Gastrointestinal and Liver Diseases, 2019
Prolonged carriage of an enteropathogen is well-recognized in bacterial, viral, protozoal and helminth intestinal infections. Asymptomatic carriage of Salmonella spp. is probably the most common example of carriage of a bacterial enteropathogen. In the majority of patients, stool cultures become negative within 12 weeks but, in some stool cultures, may remain positive for 6-12 months or longer. This human reservoir of infection is particularly important in food handlers, healthcare workers and workers in day-care centres. Eradication of Salmonella spp. can be achieved in more than 80% of cases by administration of amoxycillin or a quinolone for 4-6 weeks at standard doses. Long-term asymptomatic carriage is also recognized to occur with many other bacterial enteropathogens including Camplyobacter jejuni, Yersinia enterocolitica and Clostridium difficile.
Aeromonas
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Chi-Jung Wu, Maria José Figueras, Po-Lin Chen, Wen-Chien Ko
In Aeromonas gastroenteritis, oral ingestion of contaminated foods or water is the presumed route of infection.1 Both healthy individuals and those with underlying diseases are susceptible to Aeromonas gastroenteritis.2,37,42–44,59–61 Consumption of untreated water and recent antimicrobial therapy had been reported as associated factors in the late 1980s.59,62 Aeromonads can be the causative agent of traveler's diarrhea, particularly among those traveling to developing countries.37 Concurrent infections with other enteropathogen(s) are not uncommon.37,42,59,60
Pathobionts: mechanisms of survival, expansion, and interaction with host with a focus on Clostridioides difficile
Published in Gut Microbes, 2021
Harish Chandra, Krishna Kant Sharma, Olli H. Tuovinen, Xingmin Sun, Pratyoosh Shukla
It is widely known that microbiota protect against enteropathogen infections. In contrast, how enteropathogens may play a role in dysbiosis of the gut microbiota is poorly understood. Embedded in a matrix of extracellular polymeric substances in the intestinal mucus, gut microbiota predominantly consist of a complex of poly-microbial biofilms, which may disperse free-swimming bacteria as well.38 Pathobionts under conditions of a physiological disturbance may slough off from the biofilms, thus leading to inflammation. It has been observed that the inflammatory IBD complications in patients are exacerbated after enteropathogen infections due to dysbiotic gut.11 Enteropathogens such as Giardia duodenalis perturb the beta diversity of the microbiota and increase the abundance of Firmicutes like Clostridiales by disrupting the microbial biofilm polysaccharide matrix, thereby releasing the pathobiont.11,38 There are other enteropathogens like Campylobacter jejuni that has been shown to activate latent virulence genes of fimbriae, flagella, and hemolysin E in noninvasive E. coli, thus facilitating adherence and translocation through the epithelial barrier.39
Antimicrobial resistance in enteric bacteria: current state and next-generation solutions
Published in Gut Microbes, 2020
M. J. Wallace, S. R. S. Fishbein, G. Dantas
Within this review, the major enteropathogenic bacterial species are bifurcated into two groups: (1) invasive enteropathogens, which originate from an outside environmental reservoir, and (2) pathobionts, which originate from commensal gut species (Table 1). There are, of course, well-documented deviations from these delineations. For example, we categorize Clostridioides difficile as an invasive enteropathogen, yet it can colonize some hosts asymptomatically.46 Conversely, we classify Escherichia coli as a pathobiont, although some pathotypes of E. coli (discussed further below) are obligate invasive enteropathogens.4 The “switch” between these two categories can often be achieved rapidly through horizontal gene transfer (HGT) of genetic elements such as pathogenicity islands,47 which is discussed in Part II. It is important to note that across these pathogens, there are a range of ad hoc clinical diagnostic standards for determining susceptibility,48 and these practices are often absent or underutilized in the case of anaerobic pathogens such as Clostridioides or Bacteroides species.49
The bacterial siderophore enterobactin confers survival advantage to Salmonella in macrophages
Published in Gut Microbes, 2019
Piu Saha, Xia Xiao, Beng San Yeoh, Qiuyan Chen, Bhuvana Katkere, Girish Soorappa Kirimanjeswara, Matam Vijay-Kumar
Salmonella is a food-borne enteropathogen from the Enterobacteriaceae family of Gram-negative bacteria. The majority of Salmonella infections result in self-limiting gastroenteritis and diarrhea; however, the dissemination of this pathogen into systemic circulation often leads to life-threatening septicemia. As an intracellular pathogen, Salmonella has the machinery to invade the gut epithelia and MΦs, with the latter serving as the carrier to spread the infection systemically. After being engulfed by the MΦs, the Salmonella resides in a modified phagosome known as the Salmonella-containing vacuoles. Several mechanisms, which permit Salmonella to survive within the MΦs, have been documented, including blocking the fusion of lysosome with the Salmonella-containing vacuoles.11 The intracellular survival of Salmonella has also been purported to be dependent on its ability to exploit and utilize the diverse nutrients in the MΦs12, especially iron, which is essential for Salmonella growth and replication.13