Lecithinase

Pathogenicity and Virulence

Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022

Lola Winter

Collagenase produced by the anaerobe C. perfringens, an agent of gas gangrene, breaks down collagen in connective tissue. Lecithinase, another enzyme produced by this bacterium, lyses host cells. The resulting destruction of tissue creates an anaerobic environment for the growth of the bacteria and enhances their spread.

Bacteriology of Ophthalmic Infections

Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019

Arumugam Priya, Shunmugiah Karutha Pandian

Low oxidation-reduction potential within eye provides suitable environment for the growth of anaerobes especially P. acnes. Persistent intracellular localization of P. acnes and its secretory metabolites and enzymes will result in tissue damage (Csukas et al., 2004). Hemolytic and cytotoxic activity of P. acnes has been reported. Various enzymes such as Chondroitin sulfatase, hyaluronidase, gelatinase, phosphatase, lecithinase, and hemolysin production are found in P. acnes, which potentiate its virulence (Hoeffler, 1977). The enzyme chondroitin sulfatase initiates hydrolysis of sulfate groups from N-acetyl-D-galactosamine 6-sulfate and keratan sulfate, which are structural carbohydrates of corneal tissue. Hyaluronidase hydrolyses the nonsulfated glycosaminoglycan, the hyaluronic acid of connective tissues. The enzyme lecithinase is a type of phospholipase, which can act on lecithin and cause hemolysis (Figure 11.5).

Published in Ronald M. Atlas, James W. Snyder, Handbook Of Media for Clinical Microbiology, 2006

Ronald M. Atlas, James W. Snyder

Use: For the isolation, cultivation, and differentiation of Clostridium species based on lecithinase production and lipase production. Bacteria that produce lecithinase appear as colonies surrounded by a zone of insoluble precipitate. Bacteria that produce lipase appear as colonies with a pearly iridescent sheen.

Stenotrophomonas maltophilia – a low-grade pathogen with numerous virulence factors

Published in Infectious Diseases, 2019

Angelina Trifonova, Tanya Strateva

Genes encoding for non-haemolytic phospholipase C (lecithinase) and class D phospholipases have been identified in the S. maltophilia genome [9]. Phospholipases hydrolyse phospholipids into fatty acids and contribute to virulence with their ability to destroy cell membranes, but the pathogenic mechanisms are highly variable among different bacterial species [12,36]. They are a virulence factor in some glucose non-fermenting Gram-negative bacteria such as Pseudomonas aeruginosa [37] and Burkholderia pseudomallei [38]. Phospholipases enable pathogens to enter the host cells and tissues and affect normal cell function. As virulence factors, they are involved in destruction of protective molecules or structures such as mucus, lipoprotein membranes and immunoglobulins [10]. Phospholipase activity has only been reported for clinical S. maltophilia isolates from the trachea and the liver, according to the study by Figueirêdo et al. The authors established lecithinase activity only in strains with simultaneous haemolytic activity [10]. Travassos et al. detected phospholipase C in very low amounts in all clinical strains tested, but recognized the involvement of the enzyme in pathogenesis [12]. A recent study found no lecithinase producers in urine isolates, and variable enzyme activity (43.5–100%) in isolates from other clinical samples (tracheal aspirate, blood, cerebrospinal fluid, sputum and wound) [33].

Evaluation of gallstone classification and their diagnosis through serum parameters as emerging tools in treatment: a narrative review

Published in Postgraduate Medicine, 2022

Bhavna Sharma, Shubha Rani Sharma

Bacteria also play a major role in gallstone formation. The presence of bacteria was seen in bile as well as gallstones and this motivated the scientists to explore the relationship between bacteria and the formation of gallstones. β- glucuronidase produced by the bacteria leads to the metabolization of the conjugated bile into the unconjugated form which then precipitates and serves as a nidus for the formation of pigmented gallstones [10]. But this mechanism was not limited to pigmented gallstones. In 1998 Wu et al., reported the presence of bacteria in cholesterol gallstones after they were analyzed using a Scanning electron Microscope (SEM). The bacterial factors that pave way for gallstone formation were reported by Stewart in 2006 and these included beta-glucuronidase, Phospholipase phospholipase, urease, and slime – producing properties [11]. The urease activity of bacteria leads to the hydrolysis of urea into calcium carbonate and urea [12]. Cholesterol gallstones are formed when calcium carbonate precipitates [11]. The presence of lecithinase enzyme was seen in certain bacteria which lead to the metabolism of lecithin. Having adequate knowledge about the bile salt pool concerning the gastrointestinal and hepatobiliary equilibrium may be helpful in the designing of therapeutic strategies to alter the gallbladder’s microbiome. Gram-positive bacteria, as well as, Klebsiella were cultured from cholesterol gallstones. The Gram-negative and Gram-positive bacteria cultured from gallstones had carbohydrate and protein metabolizing genes respectively. A study was conducted in Colombo of 100 gallstone samples and it was reported that 20% of the samples had the presence of bacteria. In most of the cases, E. coli was detected, next was the Klesbsiella spp. followed by Enterobacter spp. Most commonly, aerobes isolated from gallstones include E. coli, Enterobacter faecalis etc but in some cases, anaerobes have also been isolated which include Clostridium spp., Propioni bacteria and Bacteroides fragilis. With increasing age, the risk of infection increases (>60 years). In another study, bacterial β-glucuronidase activity was reported for the formation of pigmented gallstones. Also, the involvement of bacterial urease activity was seen in slime production and nucleation during gallstone solidification [12,13]. Further reinvestigations are required for the exploration of the possible role of bacteria and its various properties in the formation and solidification of gallstones [14].