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Mycobiome in health and disease
Published in Mahmoud A. Ghannoum, John R. Perfect, Antifungal Therapy, 2019
Najla El-Jurdi, Jyotsna Chandra, Pranab K. Mukherjee
Recently, we used Ion-Torrent sequencing to characterize the gut bacteriome and mycobiome of patients with CD and their non-diseased first-degree relatives (NCDR) in 9 familial clusters living in Northern France/Belgium and in healthy individuals from 4 families living in the same area (non-CD unrelated, NCDU) [60]. CD and NCDR groups clustered together in the mycobiome but not in bacteriome profile. Microbiota of familial (CD, NCDR) samples were distinct from that of non-familial (NCDU) samples. Abundance of Serratia marcescens and Escherichia coli were high in CD patients, while that of beneficial bacteria was decreased. Abundance of C. tropicalis was significantly higher in CD compared to NCDR (p = 003) and positively correlated with S. marcescens and E. coli (Figure 32.1), with levels of ASCA. The biomass and thickness of triple species biofilms were significantly higher than single and double species biofilm (Figure 32.2a and b). C. tropicalis biofilms comprised of blastospores, while double and triple species biofilms were enriched in hyphae and exhibited close interactions, as shown by transmission electron microscopy (Figure 32.2c–e). These findings are also supported by other studies showing that members of a family share genetics, environment, diet, and bacterial microbiota, and that family members are more similar to each other than they are to unrelated individuals [61,62]. Since C. tropicalis is also known to interact with specific immune pathways [63], it is possible that microbial dysbiosis may exacerbate the disease in CD patients by modulating metabolic and host immune response pathways.
Carbenicillin, Carindacillin, Carfecillin, and Ticarcillin
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
Other Gram-negative aerobic bacteria exhibit similar susceptibility to carbenicillin and ticarcillin (Sutherland et al., 1971). Compared with ampicillin, carbenicillin and ticarcillin have a relatively high activity against Proteus vulgaris, Providencia rettgeri, and Morganella morganii (see Table 9.1). Their activity against other Gram-negative bacteria is similar to that of ampicillin (see Chapter 5, Ampicillin and amoxicillin); they are effective to a degree against Escherichia coli, P. mirabilis, salmonellae, and shigellae as well as Haemophilus influenzae, Neisseria meningitidis, and N. gonorrhoeae. Ampicillin is preferred for treatment of infections due to these bacteria because it is the more active drug. Carbenicillin and ticarcillin have some activity against ampicillin-resistant H. influenzae strains, but this activity is less (MIC 4–32 μg/ml) than their activity against ampicillin-sensitive strains (MIC 0.25–1.0 μg/ml) (Kammer et al., 1975; Thornsberry et al., 1976). Klebsiella spp. are almost invariably resistant to carbenicillin and ticarcillin, but some strains of Enterobacter spp. are relatively sensitive (Standiford et al., 1969; Sutherland et al., 1971). Some Serratia marcescens strains are susceptible to these drugs in relatively low concentrations (25 μg/ml); others are either highly resistant (MIC > 8000 μg/ml) or moderately resistant (MIC < 2000 μg/ml) (Sutherland et al., 1971; Hewitt and Winters, 1973). In a study in French outpatients (Quentin et al., 2004), resistance to ticarcillin in Enterobacteriaceae varied between 100% in strains of Klebsiella spp. and Y. enterocolitica and 22% in Proteus spp.; 42% of 1902 isolates of E. coli were resistant to ticarcillin.
Enhancing efficacy of existing antibacterials against selected multiple drug resistant bacteria using cinnamic acid-coated magnetic iron oxide and mesoporous silica nanoparticles
Published in Pathogens and Global Health, 2022
Noor Akbar, Muhammad Kawish, Tooba Jabri, Naveed Ahmed Khan, Muhammad Raza Shah, Ruqaiyyah Siddiqui
Among multiple drug resistance (MDR) bacteria, Escherichia coli and Methicillin-resistant Staphylococcus aureus (MRSA) cause several infections including gastroenteritis, meningitis, urinary tract infections (UTIs), skin, respiratory, and other nosocomial infections [11–13]. Pseudomonas aeruginosa being a nosocomial pathogen causes 20% of hospital-acquired infections, bloodstream infections and is prevalent in patients with acute leukemia, burn wounds, cystic fibrosis, and organ transplants [14,15]. Serratia marcescens colonizes the intensive care unit and causes opportunistic infections [16]. A wide spectrum of invasive infections are caused by Klebsiella pneumonia including pneumonia, meningitis, pyogenic liver abscess, UTIs, bloodstream infection, and intra-abdominal infection etc [17]. Streptococcus pneumoniae causes pneumonia in children and has been isolated from patients with purulent pleuritis [18].
Plumbagin inhibits quorum sensing-regulated virulence and biofilms of Gram-negative bacteria: in vitro and in silico investigations
Published in Biofouling, 2021
Faizan Abul Qais, Mohammad Shavez Khan, Iqbal Ahmad, Fohad Mabood Husain, Abdulaziz Abdullah Al-kheraif, Mohammed Arshad, Pravej Alam
QS is a bacterial cell-to-cell communication system in which bacteria coordinate the expression of certain sets of genes. Bacteria synthesize signal molecules (autoinducers (AIs)) which are sensed or detected by the bacteria. Once the concentration of AIs reaches the threshold level, bacteria start the expression of QS-controlled genes. The expression of most of the drug-resistant and virulent genes is controlled by QS (Ng and Bassler 2009). Acylated homoserine lactones (AHLs) are the most common AIs in Gram-negative bacteria. In QS of Gram-negative bacteria, AIs are synthesized and diffuse out of the cell; AIs bind with specific receptors to start the expression of QS-controlled genes, and this process continues by a feed-forward loop (Papenfort and Bassler 2016). There are three main QS systems in Pseudomonas aeruginosa: RhlI-RhlR, PQS-MvfR and LasI-LasR (Lee and Zhang 2015). RhlR/RhlI senses C4-HSL and the AIs for the LasR/LasI system is 3O-C12-HSL. Serratia marcescens is an opportunistic Gram-negative bacterial pathogen which is known to cause numerous nosocomial infections, including respiratory tract infection, urinary tract infections and wound infections. The severity of such infection is enhanced by the production of virulence factors that causes damage to the host’s cells (Hejazi and Falkiner 1997).
In vitro anti-biofilm efficacy of sanguinarine against carbapenem-resistant Serratia marcescens
Published in Biofouling, 2021
Yuting Fu, Wanting Liu, Miao Liu, Jianing Zhang, Min Yang, Ting Wang, Weidong Qian
Serratia marcescens is a Gram-negative opportunistic human pathogen belonging to the family Enterobacteriaceae, which causes hospital-acquired infections and outbreaks in severely immunocompromised or critically ill patients, especially those in intensive care units (ICUs) (Cristina et al. 2019). Furthermore, S. marcescens is known to cause a growing number of severe nosocomial infections, such as urinary tract infections, respiratory tract infections, bacteremia, conjunctivitis, endocarditis, meningitis, and wound infections (Su et al. 2003). S. marcescens may be generally isolated from various samples such as lung, blood, urine, and pus samples as well as from the hospital environment and medical equipment (Khanna et al. 2013). The emergence of carbapenem-resistant S. marcescens (CRSM) can generate intrinsic and/or acquired resistance to antimicrobial agents, and poses an important clinical issue (Nordmann et al. 2011). Carbapenem resistance in S. marcescens has been historically and mainly associated with a specific group of carbapenemases, including class A (mainly KPC), and class B (VIM, NDM, and IMP) (Miao et al. 2018). In recent years, a significant increase in outbreaks associated with extended-spectrum CRSM isolates has been noted in different regions of the world (Merkier et al. 2013).