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Although S. epidermidis is not usually pathogenic, patients with compromised immune systems are at risk of developing infection. These infections are generally hospital-acquired. [4] S. epidermidis is a particular concern for people with catheters or other surgical implants because it is known to form biofilms that grow on these devices. [5]
Starting very early, research into biofilm formation in Staphylococcus epidermidis has served as a model for other staphylococci such as Staphylococcus aureus and other CoNS species. Moreover, data also showed that S. capitis have a strain (AYP1020) that researchers use to general genomic characteristics compared to S. epidermidis’ strain ...
During atopic dermatitis flares, population levels of S. epidermidis has been shown to increase as an attempt to control S. aureus populations. [40] [44] Low gut microbial diversity in babies has been associated with an increased risk of atopic dermatitis. [45] Infants with atopic eczema have low levels of Bacteroides and high levels of Bacillota.
The S. haemolyticus strain JCSC1435 genome contains a 2,685,015 bp chromosome and three plasmids of 2,300 bp, 2,366 bp, and 8,180 bp. The chromosome is comparable in size to those of S. aureus and S. epidermidis and contains a similar G+C content. In addition, a large proportion of the open reading frames (ORFs) are conserved across all three ...
Microbial mats and less complex types of biofilm are found at temperature ranges from –40 °C to +120 °C, because variations in pressure affect the temperatures at which water remains liquid. [3] They even appear as endosymbionts in some animals, for example in the hindguts of some echinoids. [10]
Serratia marcescens is a fairly common opportunistic pathogen that can form biofilms on various surfaces, including medical devices such as catheters and implants, as well as natural environments like soil and water. The formation of biofilms by S. marcescens is a serious concern because of its ability to adhere to and colonize surfaces ...
The formation of biofilm and structure of EPS share a lot of similarities with bacterial ones. The formation of biofilm starts with reversible absorption of floating cells to the surface. Followed by production of EPS, the adsorption will get irreversible. EPS will colonize the cells at the surface with hydrogen bonding.
Dispersin B is produced by Aggregatibacter actinomycetemcomitans, a Gram-negative oral bacterium, when it needs to detach and disperse adherent bacterial cells. [4] A. actinomycetemcomitans forms asymmetric biofilm lobed colonies that release single cells or small clusters of bacterial cells, which can attach to nearby surfaces, form new colonies, and enable the biofilm to spread.