scholarly journals Microbial Pathogenesis

2021 ◽  
Vol 11 (12) ◽  
pp. 217-219
Author(s):  
Ruvin Haidar

For a pathogenic microbe to cause disease in a susceptible host, it must gain access to that host first. The pathogenicity of a microbe is determined by the virulence factors alongside other innate mechanisms. Apart from the initiation of infection, these virulence factors also enable the pathogenic microorganism to survive in the new environment within the susceptible host. They also enable the pathogenic microorganism to invade the host, colonize, and evade the host defense mechanisms. These virulence factors include; invasins, capsules, siderophores, adhesins, enzymes, endotoxins, and exotoxins. Key words: Pathogenicity factors and Pathological effect on cells.

2022 ◽  
Vol 23 (2) ◽  
pp. 948
Author(s):  
Urszula Wójcik-Bojek ◽  
Barbara Różalska ◽  
Beata Sadowska

The main purpose of this review is to present justification for the urgent need to implement specific prophylaxis of invasive Staphylococcus aureus infections. We emphasize the difficulties in achieving this goal due to numerous S. aureus virulence factors important for the process of infection and the remarkable ability of these bacteria to avoid host defense mechanisms. We precede these considerations with a brief overview of the global necessitiy to intensify the use of vaccines against other pathogens as well, particularly in light of an impasse in antibiotic therapy. Finally, we point out global trends in research into modern technologies used in the field of molecular microbiology to develop new vaccines. We focus on the vaccines designed to fight the infections caused by S. aureus, which are often resistant to the majority of available therapeutic options.


2009 ◽  
Vol 7 (S1) ◽  
pp. S2-S18 ◽  
Author(s):  
Arturo Casadevall ◽  
Liise-anne Pirofski

The virulence factor concept has been a powerful engine in driving research and the intellectual flow in the fields of microbial pathogenesis and infectious diseases. This review analyzes virulence factors from the viewpoint of the damage–response framework of microbial pathogenesis, which defines virulence factor as microbial components that can damage a susceptible host. At a practical level, the finding that effective immune responses often target virulence factors provides a roadmap for future vaccine design. However, there are significant limitations to this concept, which are rooted in the inability to define virulence and virulence factors in the absence of host factors and the host response. In fact, this concept appears to work best for certain types of bacterial pathogens, being less well suited for viruses and commensal organisms with pathogenic potential.


2001 ◽  
Author(s):  
Lorraine Sordillo ◽  
Don Wojchowski ◽  
Gary Perdew ◽  
Arthur Saran ◽  
Gabriel Leitner

Staphylococcus aureus is a major cause of mastitis in dairy cattle. The organism is able to adhere to and penetrate mammary epithelium, forming deep seated abscesses that result in chronic infections. This study was based on the observation that certain genotypes of S. aureus are isolated more frequently from field cases of bovine mastitis than others and the most prevalent genotypes of S. aureus have an increased ability to resist neutrophil phagocytosis and killing compared to the rare variants. It was hypothesized that these predominating genotypes differentially express virulence factors that allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. The overall objective of this study was to determine the mechanisms by which predominating S. aureus genotypes were able to resist mammary gland defense mechanisms. The following specific aims were accomplished to address the overall objectives of this project: 1. Analyze and compare cell surface and secreted protein profiles of common and rare S. aureus genotypes isolated from field cases of bovine mastitis. 2. Purify and sequence selectively synthesized proteins unique to the most prevalent genotypes of S. aureus . 3. Determine the in vitro effects of isolated proteins on essential host defense mechanisms. Results from each specific aim showed that these redominating genotypes differentially express factors that may allow them to overcome or suppress essential host defense mechanisms and successfully colonize mammary parenchyma. Using complementary approaches, both the US and Israeli teams identified differentially expressed S. aureus factors that were positively correlated with virulence as determined by the ability to modify host immune cell responses and increase disease pathogenesis. Several candidate virulence factors have ben identified at both the molecular (US team) and protein (Israeli team) levels. Components of the phosphotransferase system were shown to be differentially expressed in prevalent strains of S. aureus and to modify the growth potential of these strains in a milk microenvironment. Evidence provided by both the Israeli and US teams also demonstrated a potential role of Staphylococcal enterotoxins in the pathogenesis of mastitis. Certain enterotoxins were shown to directly affect neutrophil bactericidal activities which can profoundly affect the establishment of new intramammary infections. Other evidence suggests that S. aureus superantigens can suppress mammary defenses by enhancing lymphoid suppressor cell activity. Collectively, these data suggest that unique factors are associated with predominating S. aureus genotypes that can affect in vitro and in vivo virulence as related to the pathogenesis of bovine mastitis. The potential development of a subunit mastitis vaccine which incorporates only relevant antigenic determinants has not been investigated in depth. Experiments outlined in this proposal has identified putative virulence factors which contribute to the pathogenesis of S. aureus mastitis and which may be used to formulate an efficacious subunit mastitis vaccine. Results from these studies may lead to the development of new methods to prevent this costly disease, providing a viable alternative to less effective mastitis control procedures based on chemotherapy.


2017 ◽  
Vol 6 (05) ◽  
pp. 5373
Author(s):  
Prabha Ponnusamy* ◽  
Radhika Katragadda ◽  
Thyagarajan Ravinder

Asymptomatic bacteriuria (ASB), most common during pregnancy is endangering as it may lead to maternal and fetal complications. Various organisms causing ASB combats the host defense mechanisms through virulence factors exhibited by them. In order to understand the pathogenesis and sequelae of infections, virulence factors like hemolysin production, gelatinase production, haemagglutination, biofilm production and many more should be identified. Hence, we aimed at studying the distribution of virulence factors among each organism causing asymptomatic bacteriuria in pregnant females attending a tertiary care hospital. Materials and Methods: This cross-sectional study was conducted in Department of Microbiology over a period of one year and six months (January 2014 to June 2015) at a tertiary care teaching hospital. A total of 1000 urine samples were included in study taken from pregnant women with asymptomatic bacteriuria. Isolation, identification of organisms was done according to standard microbiological techniques and virulence factors for individual organisms by phenotypic method were tested. Results: Out of 1000 samples screened for ASB, organisms were isolated in following frequency distribution: Escherichia coli, the commonest 54/118 (45.76%), Klebsiella pneumoniae 21/118 (17.80%), Staphylococcus aureus 19/118 (16.10%), Staphylococcus saprophyticus 10/118 (8.45%), Enterococcus faecalis 9/118 (7.63%), Pseudomonas aeruginosa 3/118 (2.54%) and Proteus mirabilis 2/118 (1.69%). Virulence factors for individual organisms and biofilm detection for all organisms were done. Conclusion: Multifactorial mechanisms determine the pathogenicity of an organism and it needs to be explored by analyzing each virulence factor and mechanism of invasion in combating the host defense systems. Hence analyzing the phenotypic expression of each virulence factor helps in better understanding about the complications of ASB.


1975 ◽  
Vol 48 (5) ◽  
pp. 706-720 ◽  
Author(s):  
M. Schutte ◽  
R. DiCamelli ◽  
P. Murphy ◽  
M. Sadove ◽  
H. Gewurz

2021 ◽  
Vol 22 (5) ◽  
pp. 2566 ◽  
Author(s):  
Barbara Ruaro ◽  
Francesco Salton ◽  
Luca Braga ◽  
Barbara Wade ◽  
Paola Confalonieri ◽  
...  

Alveolar type II (ATII) cells are a key structure of the distal lung epithelium, where they exert their innate immune response and serve as progenitors of alveolar type I (ATI) cells, contributing to alveolar epithelial repair and regeneration. In the healthy lung, ATII cells coordinate the host defense mechanisms, not only generating a restrictive alveolar epithelial barrier, but also orchestrating host defense mechanisms and secreting surfactant proteins, which are important in lung protection against pathogen exposure. Moreover, surfactant proteins help to maintain homeostasis in the distal lung and reduce surface tension at the pulmonary air–liquid interface, thereby preventing atelectasis and reducing the work of breathing. ATII cells may also contribute to the fibroproliferative reaction by secreting growth factors and proinflammatory molecules after damage. Indeed, various acute and chronic diseases are associated with intensive inflammation. These include oedema, acute respiratory distress syndrome, fibrosis and numerous interstitial lung diseases, and are characterized by hyperplastic ATII cells which are considered an essential part of the epithelialization process and, consequently, wound healing. The aim of this review is that of revising the physiologic and pathologic role ATII cells play in pulmonary diseases, as, despite what has been learnt in the last few decades of research, the origin, phenotypic regulation and crosstalk of these cells still remain, in part, a mystery.


2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Justyna Bien ◽  
Olga Sokolova ◽  
Przemyslaw Bozko

UropathogenicEscherichia coli(UPEC) is a causative agent in the vast majority of urinary tract infections (UTIs), including cystitis and pyelonephritis, and infectious complications, which may result in acute renal failure in healthy individuals as well as in renal transplant patients. UPEC expresses a multitude of virulence factors to break the inertia of the mucosal barrier. In response to the breach by UPEC into the normally sterile urinary tract, host inflammatory responses are triggered leading to cytokine production, neutrophil influx, and the exfoliation of infected bladder epithelial cells. Several signaling pathways activated during UPEC infection, including the pathways known to activate the innate immune response, interact with calcium-dependent signaling pathways. Some UPEC isolates, however, might possess strategies to delay or suppress the activation of components of the innate host response in the urinary tract. Studies published in the recent past provide new information regarding how virulence factors of uropathogenicE. coliare involved in activation of the innate host response. Despite numerous host defense mechanisms, UPEC can persist within the urinary tract and may serve as a reservoir for recurrent infections and serious complications. Presentation of the molecular details of these events is essential for development of successful strategies for prevention of human UTIs and urological complications associated with UTIs.


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