Disease relevance of Fusobacteria

• Erythromycin offers a reasonable therapeutic alternative to penicillin in the treatment of a penicillin-allergic patient who has a mild or moderately severe anaerobic or mixed aerobic/anaerobic infection not involving Bacteroides fragilis or fusobacteria [1].
• Sparfloxacin was active against all strains (MIC for 90% of strains tested, < or = 1 micrograms/ml) except for most fusobacteria and one-third of the Prevotella spp [2].
• Using a proposed breakpoint of 0.5 mg/L, these studies showed that gemifloxacin had generally higher potency against Gram-positive anaerobes (Clostridium perfringens, all Peptostreptococcus spp.) and fusobacteria (Fusobacterium nucleatum, Fusobacterium necrophorum) and moderate but variable potency against Gram-negative anaerobes [3].
• No impact on peptostreptococci, lactobacilli, Veillonella, Bacteroides or fusobacteria was observed, while bifidobacteria and clostridia decreased during moxifloxacin administration [4].
• In contrast to antibiotic-associated diarrhea pigs, bacteria belonging to Bacteroidaceae, Fusobacteria, and Enterobacteriaceae were detected as succinate producers in a non-treated pig [5].

High impact information on Fusobacteria

• Among the anaerobes tested, only fusobacteria (45%) required > or =4 microg of ABT-773/ml for inhibition [6].
• Erythromycin- and moxifloxacin-resistant fusobacteria were susceptible to GAR-936, with an MIC(90) of 0.06 microg/ml [7].
• Gemifloxacin mesylate (SB 265805) was 1 to 4 dilutions more active than trovafloxacin against fusobacteria and peptostreptococci, and the two drugs were equivalent against clostridia and P. asaccharolytica [8].
• Gemifloxacin was equivalent to sitafloxacin (DU 6859a) against peptostreptococci, C. perfringens, and C. ramosum, and sitafloxacin was 2 to 3 dilutions more active against fusobacteria [8].
• The fusobacteria were relatively resistant to all the antimicrobial agents tested except penicillin G (one penicillinase-producing strain of F. nucleatum was found) and amoxicillin clavulanate [9].

Chemical compound and disease context of Fusobacteria

• beta-Lactamase production (nitrocefin disk method) and agar dilution susceptibility of amoxicillin, amoxicillin-clavulanate, ticarcillin, ticarcillin-clavulanate, cefoxitin, imipenem, and metronidazole were determined for 320 Bacteroides species (not Bacteroides fragilis group) and 129 fusobacteria from 28 U.S. centers [10].
• Although relative drug activities varied by organism, organisms relatively susceptible to one were relatively susceptible to all and organisms relatively resistant to one were relatively resistant to all; an exception was fusobacteria, which were usually susceptible only to azithromycin [11].
• For the beta-lactamase-positive fusobacteria, greater than or equal to 97% were susceptible to amoxicillin-clavulanate, ampicillin-sulbactam, cefoperazone-sulbactam, trospectomycin, and cefoxitin, 90% were susceptible to cefotetan, and 89% were susceptible to tosufloxacin [12].
• Coaggregations of fusobacteria with the 63 gram-negative strains were usually inhibited by EDTA, whereas those with the 27 gram-positive strains were usually not inhibited [13].
• Heat treatment of many of the gram-negative partners not only enhanced their coaggregation with the fusobacteria but also changed lactose-sensitive coaggregations to lactose-insensitive coaggregations [13].

Biological context of Fusobacteria

• 1. The idea that fermentation acids could prevent the enrichment of fusobacteria in vivo was supported by the observation that dietary lysine supplementation did not enhance the lysine deamination rate of the mixed ruminal bacteria [14].

Gene context of Fusobacteria

• The pKH9 rep gene is not present in this fragment, suggesting that pKH9 can replicate in fusobacteria independently of the Rep protein [15].
• With both fusobacteria IL-1 was present in the intracellular environment, whereas the predominant secretory product was either IL-1 or an IL-1 inhibitor [16].
• Furthermore, the fusobacteria were usually inactivated by proteinase K treatment, and the treponemes were not affected [17].
• None of the patients harboured beta-lactamase producing fusobacteria on the day of admission [18].

References