Deep Neck Space Infection
Firza Alexander Gronthoud in Practical Clinical Microbiology and Infectious Diseases, 2020
The microbiological pattern of DNSIs is generally polymicrobial, including aerobes and anaerobes. The predominant anaerobic organisms are Prevotella spp., Porphyromonas spp., Fusobacterium spp., and Peptostreptococcus spp.; aerobic organisms are group A Streptococcus, viridans streptococci, Staphylococcus aureus and Haemophilus influenzae. More than two-thirds of deep neck infections contain β-lactamase-producing bacteria.
Gemifloxacin
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
MIC50s and MIC90s of gemifloxacin against Bacteroides fragilis range from 0.5–1 and from 0.5–16 µg/ml (most ≥ 2 µg/ml), respectively (Cormican and Jones, 1997; Marco et al., 1997; Wise and Andrews, 1999; Goldstein, 2000; King et al., 2000; Kleinkauf et al., 2001). MIC90s of ≥ 4 µg/ml have been recorded for the following Bacteroides spp.: B. caccae, B. distasonis, B. ovatus, B. thetaiotaomicron, B. uniformis, and B. vulgatus (Goldstein et al., 1999a). Goldstein et al., (1999a, b) reported lower MIC90s for B. gracilis (1 µg/ml), B. stercoralis (0.5 µg/ml), B. tectum (0.25 µg/ml), and B. urealyticus (2 µg/ml). Prevotella spp. (MIC90s, 0.5–16 µg/ml) and Veillonella spp. (MIC90, 8 µg/ml) are relatively insensitive to gemifloxacin (Marco et al., 1997; Goldstein et al., 1999a; Goldstein et al., 1999b; King et al., 2000; Kleinkauf et al., 2001). Gemifloxacin is more potent against Porphyromonas spp., with MIC90s, ≤ 0.25 µg/ml (Goldstein et al., 1999b) or 1 µg/ml (King et al., 2000). MIC90s against Fusobacterium spp. are generally ≥ 2 µg/ml (Goldstein, 2000), although values of 0.25–1 µg/ml have also been recorded (Goldstein et al., 1999a; King et al., 2000; Kleinkauf et al., 2001). Gemifloxacin is more potent than ciprofloxacin or levofloxacin against Clostridium perfringens with MIC90s of 0.06–0.12 µg/ml (Goldstein et al., 1999a; Wise and Andrews, 1999). Gemifloxacin MIC90s against C. difficile are elevated (2 to > 16 µg/ml), but in most studies other Clostridium spp. are more susceptible, with MIC90 values from 0.5 to 2 µg/ml (Goldstein et al., 1999a; Goldstein et al., 1999b; Wise and Andrews, 1999; Goldstein, 2000; King et al., 2000). Most studies indicate that Peptostreptococcus spp. are inhibited by gemifloxacin with MIC90s ≤ 0.25 µg/ml, although other studies report MIC90s of 0.5–4 µg/ml (Cormican and Jones, 1997; Goldstein et al., 1999a; Goldstein et al., 1999b; Wise and Andrews, 1999; King et al., 2000).
Diagnosis of pleural empyema/parapneumonic effusion by next-generation sequencing
Published in Infectious Diseases, 2021
Yoshiki Shiraishi, Kirill Kryukov, Katsuyoshi Tomomatsu, Fumio Sakamaki, Shigeaki Inoue, So Nakagawa, Tadashi Imanishi, Koichiro Asano
The predominant bacteria identified by NGS matched the culture results in five effusions (Table 2). In contrast, the predominant bacteria identified in three effusions by NGS did not match those identified by culture. In an effusion that was positive for Peptostreptococcus sp. and Campylobacter curvus in culture, these bacteria represented only 0.01% and 1.6% of the total bacterial genomes, respectively, whereas NGS identified the anaerobes, Porphyromonas endodontalis (25%), Fusobacterium nucleatum (21%), and Prevotella oris (16%). In the other two effusions, culture-positive Streptococcus anginosus and Pseudomonas aeruginosa, accounted for only 0.9% and 0.2% of the total bacterial genomes, respectively. Prevotella oris (77%) and F. nucleatum (89%) were the predominant bacteria according to NGS in these samples.
Streptogramins for the treatment of infections caused by Gram-positive pathogens
Published in Expert Review of Anti-infective Therapy, 2021
Sophie Reissier, Vincent Cattoir
The spectrum of activity of streptogramins includes a broad range of aerobic and anaerobic Gram-positive bacteria, with a MIC90 generally ≤1 mg/l Table 2 [28–33]. They are active against methicillin-susceptible, MRSA, and most of E. faecium isolates (including VREF) Table 2 [30,34]. Noteworthy, Enterococcus faecalis is a gap in the antimicrobial spectrum since this Gram-positive species is intrinsically resistant to type A streptogramins (phenotype LSA, which results in lincosamide and streptogramins A resistance) and to the A plus B streptogramin combinations, due to the presence of the lsa(A) gene [35–37]. Streptogramins are also active against S. pneumoniae (regardless of resistance to β-lactams and macrolides), β-hemolytic streptococci, viridans streptococci, Corynebacterium spp., and Listeria monocytogenesTable 2 [28,38,39]. In addition, streptogramins exhibit activity against most of Gram-positive anaerobes, such as Actinomyces spp., Clostridium spp., Lactobacillus spp., Peptostreptococcus spp., and Cutibacterium acnesTable 2 [33,39]. They are also active against Mycoplasma spp., Ureaplasma urealyticum, and Chlamydia spp. Indeed, European guidelines about M. genitalium infections recommend pristinamycin as third-line therapy in patients failing both azithromycin and moxifloxacin therapy [40,41]. Interestingly, they also have a good activity against fastidious Gram-negative bacteria including Moraxella catarrhalis, Neisseria spp., and Legionella pneumophila (Table 2) [28,38,39]. Streptogramins have a variable activity against Bacteroides fragilis group and other Gram-negative anaerobes. Several strains are resistant and some, like Fusobacterium spp. are very susceptible (Table 2) [28,39,40]. Finally, Enterobacterales, Pseudomonas aeruginosa, and Acinetobacter spp. are intrinsically resistant to high levels of streptogramins [28].
The interplay between oral microbiota, gut microbiota and systematic diseases
Published in Journal of Oral Microbiology, 2023
Xiujun Tan, Yizhong Wang, Ting Gong
Colorectal cancer (CRC) is the third most commonly diagnosed malignancy and the second leading cause of cancer death in the world [115]. Early and convenient screening of CRC is critical. Fecal microbiota is reported to be potentially suitable for screening of CRC, with sensitivity ranging from 52.6% to 76.6% [116,117], while combining the data from fecal microbiota and oral swab microbiota, the screening sensitivity increased to 76% for CRC and 88% for polyps, with 95% specificity for both. Interestingly, gut microbiota rich in Lachnospiraceae was negatively correlated with oral pathogen colonization in the gut, suggesting that the gut microbiota protects against ectopic colonization of environmental bacteria in the bowel [118]. Oral bacteria, such as Peptostreptococcus, Streptococcus and Solobacterium spp., were at a significantly higher relative abundance in saliva and stool samples of CRC patients compared with controls, suggesting that indigenous oral bacteria may have promoted initiation of CRC carcinogenesis [119]. F. nucleatum is a Gram-negative commensal anaerobe as part of the gut and oral flora, generally found in human dental plaque. Compared to healthy controls, over-abundance of F. nucleatum was found in colorectal tissue biopsies [120] and saliva [121] in CRC patients. Identical strains of F. nucleatum were detected in their colorectal cancer and oral cavity, suggesting that F. nucleatum in CRC originates from the oral cavity [122]. Oral communities have the highest variation and the richest sequences of F. nucleatum, but only certain strains of F. nucleatum are enriched in the gastrointestinal tract, and others are diminished during translocation [123]. The hematogenous route may be the preferred way for oral F. nucleatum to reach colon tumors other than the enteral route [29]. F. nucleatum invades CRC cells and stimulates cancer growth through binding its unique FadA adhesin to E-cadherin [124]. It modulates the tumor micro-environment, confers chemoresistance and promotes CRC metastasis [125–127]. Porphyromonas asaccharolytica and P. gingivalis, which correspond to bacterial species associated with periodontal disease, are significantly increased in feces of CRC patients, and are capable of inducing cellular senescence through the secretion of butyrate in human diploid fibroblasts. These results suggest a causal relationship between Porphyromonas species overgrowth and colorectal tumourigenesis which may be due to butyrate-induced senescence [128].
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