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Clindamycin and Lincomycin
Published in 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, Kucers’ The Use of Antibiotics, 2017
Although Clostridium difficile susceptibility to clindamycin ranges from 10% to as high as 90% in various studies, this organism is basically considered resistant to clindamycin (Levett, 1988; Buchler et al., 2014). During outbreaks of diarrhea linked with C. difficile, the isolates are typically clindamycin-resistant. Clostridium tetani and Clostridium perfringens are susceptible, as is Clostridium septicum (Gabay et al., 1981; Marchand-Austin et al., 2014). But some strains of C. perfringens as well as Clostridium sporogenes, Clostridium tertium, Clostridium bifermentans, Clostridium novyi, Clostridium ramosum, and Clostridium sordelli may be clindamycin-resistant (Dornbusch, 1977; Staneck and Washington, 1974; Sutter and Finegold, 1976; Wilkins and Thiel, 1973). Other anaerobic Gram-positive organisms, such as Peptococcus, Peptostreptococcus, Propionibacterium, and Lactobacillus species, are typically susceptible (Denys et al., 1983; Sutter and Finegold, 1976). Peptostreptococcus spp. strains resistant to clindamycin have been reported (Reig et al., 1992). Bayer et al. (1978) reported that although 39 of 40 isolates of Lactobacillus spp. were inhibited by 5 mg of clindamycin or less per liter, these concentrations were bactericidal for less than 20% of the isolates tested. Mayrhofer et al. (2010) reported a wide range of clindamycin minimum inhibitory concentration (MIC) values (concentrations generally ranged from ≤ 0.12 to 8 mg/l) against the Lactobacillus spp. with no clear observed pattern. Debate surrounding the clinical significance of Lactobacillus is ongoing (Cannon et al., 2005). Clindamycin is usually active against most isolates of Actinomycesisraelii or Bifidobacterium and Eubacterium spp. (Brook and Frazier, 1993; Holmberg et al., 1977; Sutter and Finegold, 1976).
The impact and toxicity of glyphosate and glyphosate-based herbicides on health and immunity
Published in Journal of Immunotoxicology, 2020
Cindy Peillex, Martin Pelletier
Recent studies suggest that glyphosate and GBHs interact with microorganisms and affect their interaction with the immune system. Mendler et al. (2020) studied the relationship between mucosal-associated invariant T-cells (MAIT) and gut bacteria Escherichia coli and Lactobacillus reuteri, which respectively induce and inhibit MAIT TNF and IFNγ production to control gut microbiota tolerance. Using a model with bacteria pretreated with glyphosate and subsequently cultured with MAIT, the authors showed that treated E. coli still induced the same MAIT TNF and IFNγ responses whereas treated L. reuteris increased MAIT production of TNF but not IFNγ. Hence, in this model, glyphosate reduced microbiota tolerance. A case report study described a Clostridium tertium infection after GBH ingestion for suicidal purposes in a 44-year-old woman (You et al. 2015). The authors suspected that the intestinal mucosa deterioration seen in this woman was caused by the herbicide that had allowed the bacterial infection to evolve. In conclusion, glyphosate seems to be able to disrupt interactions between bacteria and the immune system, at least at the gut interface. These changes might lead to lower microbiota tolerance or even infection development.