Faculty Opinions recommendation of Sulfide Protects Staphylococcus aureus from Aminoglycoside Antibiotics but Cannot Be Regarded as a General Defense Mechanism against Antibiotics.

2018 ◽  
Author(s):  
Robert Poole
Keyword(s):  
Staphylococcus Aureus ◽  
Defense Mechanism ◽  
Aminoglycoside Antibiotics

scholarly journals Effect of Ciprofloxacin on the Growth and Biofilm Formation Ability of Staphylococcus aureus

2021 ◽  
pp. 44-59
Author(s):  
N. Queenette, Obinaju ◽  
C. Chukwunonyerem, Ogwunga ◽  
O. Sylvia, Anyadoh-Nwadike ◽  
U. Emmanuel, Nwakwasi
Keyword(s):  
Staphylococcus Aureus ◽  
Defense Mechanism ◽  
Bacterial Flora ◽  
Protein A ◽  
Inhibitory Effect ◽  
Phenotypic Characterization ◽  
Upper Respiratory Tract ◽  
Staphylococcal Infections ◽  
Superficial Skin ◽  
Time Kill

Staphylococcus aureus is part of the normal bacterial flora of the skin, intestine and upper respiratory tract of both humans and animals and has the potential of causing staphylococcal infections if there is a breach in the hosts’ defense mechanism. These infections could range from mild superficial skin infections to more severe and even fatally invasive diseases such as sepsis and toxic shock syndrome. The infectivity of S. aureus is attributed to its ability to withstand extreme conditions and its possession of various virulence factors. The aim of this project was to study the effect of ciprofloxacin on the growth and biofilm forming ability of CM10 strain of Staphylococcus aureus using time kill study, resazurin and live/dead staining of biofilms and Real-time polymerase chain reaction. The identity of the given CM10 strain was confirmed when the result of the API-Staph was in total accordance with the results obtained from the colony morphology and phenotypic characterization tests (Coagulase/protein A, Gram, and Catalase tests). CM10 strain of S. aureus was not susceptible to 0.25mg/L of ciprofloxacin used for the time kill experiment but was susceptible to a minimum inhibitory concentration of 0.5mg/L. The difference between the ciprofloxacin treated biofilms of CM10 strain and the untreated biofilms was significant (P<0.05) showing that ciprofloxacin has an adverse effect on the cells in the biofilm. The results of this study provide an insight on the growth as well as the biofilm forming ability of CM10 strain of Staphylococcus aureus. Ciprofloxacin has been shown to be an effective antibacterial against this strain of S. aureus by its inhibitory effect on the growth as well as biofilm forming ability of this strain of S. aureus.  This information would assist in developing novel anti-biofilm therapies to help in the management of biofilm mediated infections thereby reducing the morbidity and mortality rate of staphylococcal infections.

scholarly journals The role of the msaABCR operon in implant-associated chronic osteomyelitis in Staphylococcus aureus USA300 LAC

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Gyan S. Sahukhal ◽  
Michelle Tucci ◽  
Hamed Benghuzzi ◽  
Gerri Wilson ◽  
Mohamed O. Elasri
Keyword(s):  
Staphylococcus Aureus ◽  
Virulence Factors ◽  
Biofilm Formation ◽  
Defense Mechanism ◽  
Chronic Osteomyelitis ◽  
Bone Destruction ◽  
The United States ◽  
Protease Production ◽  
Bone Necrosis ◽  
K Wires

Abstract Background The msaABCR operon regulates several staphylococcal phenotypes such as biofilm formation, capsule production, protease production, pigmentation, antibiotic resistance, and persister cells formation. The msaABCR operon is required for maintaining the cell wall integrity via affecting peptidoglycan cross-linking. The msaABCR operon also plays a role in oxidative stress defense mechanism, which is required to facilitate persistent and recurrent staphylococcal infections. Staphylococcus aureus is the most frequent cause of chronic implant-associated osteomyelitis (OM). The CA-MRSA USA300 strains are predominant in the United States and cause severe infections, including bone and joint infections. Results The USA300 LAC strain caused significant bone damage, as evidenced by the presence of severe bone necrosis with multiple foci of sequestra and large numbers of multinucleated osteoclasts. Intraosseous survival and biofilm formation on the K-wires by USA300 LAC strains was pronounced. However, the msaABCR deletion mutant was attenuated. We observed minimal bone necrosis, with no evidence of intramedullary abscess and/or fibrosis, along reduced intraosseous bacterial population and significantly less biofilm formation on the K-wires by the msaABCR mutant. microCT analysis of infected bone showed significant bone loss and damage in the USA300 LAC and complemented strain, whereas the msaABCR mutant’s effect was reduced. In addition, we observed increased osteoblasts response and new bone formation around the K-wires in the bone infected by the msaABCR mutant. Whole-cell proteomics analysis of msaABCR mutant cells showed significant downregulation of proteins, cell adhesion factors, and virulence factors that interact with osteoblasts and are associated with chronic OM caused by S. aureus. Conclusion This study showed that deletion of msaABCR operon in USA300 LAC strain lead to defective biofilm in K-wire implants, decreased intraosseous survival, and reduced cortical bone destruction. Thus, msaABCR plays a role in implant-associated chronic osteomyelitis by regulating extracellular proteases, cell adhesions factors and virulence factors. However additional studies are required to further define the contribution of msaABCR-regulated molecules in osteomyelitis pathogenesis.

scholarly journals Surgery of infrarenal inflammatory aneurysm of abdominal aorta infected with methicillin resistant Staphylococcus aureus in a patient undergoing haemodialysis

2008 ◽  
Vol 136 (9-10) ◽  
pp. 529-532 ◽  
Author(s):  
Srdjan Babic ◽  
Petar Popov ◽  
Miroslav Milicic ◽  
Nenad Ilijevski ◽  
Dragoslav Nenezic ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Abdominal Aorta ◽  
Defense Mechanism ◽  
Immune Defense ◽  
Aortic Aneurysms ◽  
Inflammatory Aneurysm ◽  
Abdominal Aortic ◽  
Inflammatory Abdominal Aortic Aneurysm

INTRODUCTION Inflammatory abdominal aortic aneurysm accounts for 5% to 10% of all cases of abdominal aortic aneurysm and differs from typical atherosclerotic abdominal aortic aneurysm in many important ways. Although both inflammatory and atherosclerotic abdominal aortic aneurysms most commonly affect the infrarenal portion of the abdominal aorta, patients with the inflammatory variant are younger and usually symptomatic, chiefly from back or abdominal pain. Unlike patients with atherosclerotic abdominal aortic aneurysm, most with the inflammatory variant have an elevated erythrocyte sedimentation rate or abnormalities of other serum inflammatory markers. Computed tomography and magnetic resonance imaging are both sensitive for demonstrating the cuff of soft tissue inflammation surrounding the aneurysm that is characteristic of inflammatory abdominal aortic aneurysm. Inflammatory abdominal aortic aneurysm can be primarily infected by degenaration of an infected artery (in less than 1% of cases), or can become secondary infected in the already existing aneurysm. Secondary infection of the pre-existing aneurysm has big influence on treatment choice, but is also rare. Clinically non-symptomatic infection, also known as bacterial collonisation, can be very frequent, regarding a greatly increased number of positive intraoperative findings (10-15%). Prolonged intravascular catheterization, vascular grafting, repeated punctures with large bore needles, and decreased immune defense mechanism make uraemic patients undergoing hemodialysis more likely to develop Staphylococcus aureus bacteraemia and its complications. CASE OUTLINE The case shows a gigantic inflammatory aneurysm of the abdominal aorta, localized infrarenally, which was solved successfully by resection of the aneurysm of the abdominal aorta, and interposition of Dacron tubular graft 22 mm. Bacterial examination of the aneurysmal sac was positive: methicillin-resistent Staphylococcus aureus was detected. CONCLUSION There were no postoperative complications, and the final outcome was fully satisfactory. Control CT scans after 3, 6 and 12 months were regular, with signs of regression fibrosis of the retroperitoneum.

scholarly journals RNA-Seq Whole Transcriptome Analysis of Bovine Mammary Epithelial Cells in Response to Intracellular Staphylococcus aureus

2020 ◽  
Vol 7 ◽  
Author(s):  
Xiaozhou Wang ◽  
Feng Su ◽  
Xiaohui Yu ◽  
Na Geng ◽  
Liping Li ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Epithelial Cells ◽  
Defense Mechanism ◽  
Mammary Epithelial Cells ◽  
Treated Group ◽  
Mammary Epithelial ◽  
Differentially Expressed ◽  
Receptor Interaction ◽  
Rna Seq ◽  
Bovine Mammary Epithelial Cells

Staphylococcus aureus (S. aureus), a common mastitis pathogen widespread in the natural environment of dairy farms, is capable of invading mammary epithelial cells making treatment difficult. However, the mechanism of the response of bovine mammary epithelial cell to S. aureus invasion remains elusive. In this study, transcriptomic analysis and bioinformatics tools were applied to explore the differentially expressed RNAs in bovine mammary epithelial cells (bMECs) between the control and S. aureus-treated group. A total of 259 differentially expressed mRNAs (DEmRNAs), 27 differentially expressed microRNAs (DEmiRNAs), and 21 differentially expressed long non-coding RNAs (DElncRNAs) were found. These RNAs mainly enrich the inflammatory response, immune response, endocytosis, and cytokine-cytokine receptor interaction. qRT-PCR was used to analyze the quality of the RNA-seq results. In particular, to the defense mechanism of bovine mammary epithelial cells against intracellular S. aureus, the PPAR signaling pathway and the genes (ACOX2, CROT, and NUDT12) were found to be up-regulated to promote the production of peroxisomes and ROS, DRAM1 expression was also up-regulated to facilitate the activation of autophagy, indicating that the above mechanisms were involved in the elimination of intracellular S. aureus in bovine mammary epithelial cells.

scholarly journals Sulfide ProtectsStaphylococcus aureusfrom Aminoglycoside Antibiotics but Cannot Be Regarded as a General Defense Mechanism against Antibiotics

2018 ◽  
Vol 62 (10) ◽  
Author(s):  
Julia Weikum ◽  
Niklas Ritzmann ◽  
Nils Jelden ◽  
Anna Klöckner ◽  
Sebastian Herkersdorf ◽  
...  
Keyword(s):  
Defense Mechanism ◽  
Model Organism ◽  
Inhibitory Effect ◽  
Aminoglycoside Antibiotics ◽  
Drug Uptake ◽  
Protective Mechanism ◽  
Bacterial Cells ◽  
Content Type ◽  
Sulfide Production ◽  
The Impact

ABSTRACTSulfide production has been proposed to be a universal defense mechanism against antibiotics in bacteria (K. Shatalin, E. Shatalina, A. Mironov, and E. Nudler, Science 334:986–990, 2011, doi:10.1126/science.1209855). To gain insight into the mechanism underlying sulfide protection, we systematically and comparatively addressed the interference of sulfide with antibiotic activity againstStaphylococcus aureus, as a model organism. The impact of sulfide and sulfide precursors on the antibiotic susceptibility ofS. aureusto the most important classes of antibiotics was analyzed using modified disk diffusion assays, killing kinetic assays, and drug uptake studies. In addition, sulfide production and the impact of exogenously added sulfide on the physiology ofS. aureuswere analyzed. Sulfide protection was found to be limited to aminoglycoside antibiotics, which are known to be taken up by bacterial cells in an energy-dependent process. The protective mechanism was found to rely on an inhibitory effect of sulfide on the bacterial respiratory chain, leading to reduced drug uptake.S. aureuswas found to be incapable of producing substantial amounts of sulfide. We propose that bacterial sulfide production should not be regarded as a general defense mechanism against antibiotics, since (i) it is limited to aminoglycosides and (ii) production levels vary considerably among species and, as forS. aureus, may be too low for protection.

Sign in / Sign up

Export Citation Format

Share Document