Laser therapy in the correction of pathogenetic disorders in pyoderma

2021 ◽  
pp. 25-30
Author(s):  
Anastasiya Olegovna Laknitskaya

Currently, one of the priority medico-social problems of medicine is the optimization of methods for treating bacterial skin infections, in particular pyoderma associated with S pyogenes - group A Streptococcus. The traditional treatment complex, which includes antibacterial drugs used systemically or locally, selected taking into account individual sensitivity and the presence of pathognomonic microflora, is not always effective due to an increase in antibiotic resistance. Currently implemented methods of immunocorrection, carried out taking into account changes in the immune status in this pathology and the corresponding clinical pictures of patients, are pathogenetically justified and can be effective. The use of local laser therapy requires laboratory approaches to diagnostics, clarifying the role of factors of innate and adaptive immunity, intercellular mediators and antioxidant defense systems, which allow optimizing laser therapy as a method of treating this pathology. The use of a 450nm low-intensity laser promotes clinical recovery in patients.

2021 ◽  
pp. 17-20
Author(s):  
O. Laknitskaya

Currently, one of the priority medical and social problems of medicine is to optimize the treatment of bacterial skin infections, in particular pyoderma associated with Streptococcus pyogenes-group A streptococcus. The traditional treatment complex, including antibacterial drugs used systemically or topically, selected taking into account individual sensitivity, the presence of pathognomonic microflora, is not always effective due to the increase in antibiotic resistance. Currently implemented methods of immunocorrection, taking into account changes in the immune status in this pathology, corresponding to the clinic of patients, are pathogenetically justified and can be effective. The use of immunomodulatory therapy requires a change in approaches to diagnosis, clarifying the role of factors of innate and adaptive immunity, intercellular mediators and the system of antioxidant protection, allowing to optimize the methods of treatment of this pathology. The use of recombinant interleukin-2 makes up for the lack of interleukin-2 in the blood serum of patients with streptoderma and contributes to the clinical recovery of patients.


2020 ◽  
pp. 64-70
Author(s):  
Anastasiya Laknitskaya

Currently, one of the priority medical and social problems is the optimization of treatment methods for pyoderma associated with Streptococcus pyogenes — group A streptococcus (GAS). To date, the proportion of pyoderma, the etiological factor of which is Streptococcus pyogenes, is about 6 % of all skin diseases and is in the range from 17.9 to 43.9 % of all dermatoses. Role of the bacterial factor in the development of streptococcal pyoderma is obvious. Traditional treatment complex includes antibacterial drugs selected individually, taking into account the antibiotic sensitivity of pathognomonic bacteria, and it is not always effective. Currently implemented immunocorrection methods often do not take into account specific immunological features of the disease, the individual, and the fact that the skin performs the function of not only a mechanical barrier, but it is also an immunocompetent organ. Such an approach makes it necessary to conduct additional studies clarifying the role of factors of innate and adaptive immunity, intercellular mediators and antioxidant defense system, that allow to optimize the treatment of this pathology.


2018 ◽  
Vol 5 (7) ◽  
Author(s):  
Sana S Ahmed ◽  
Kasey E Diebold ◽  
Jacob M Brandvold ◽  
Saadeh S Ewaidah ◽  
Stephanie Black ◽  
...  

Abstract Two consecutive outbreaks of group A Streptococcus (GAS) infections occurred from 2015–2016 among residents of a Chicago skilled nursing facility. Evaluation of wound care practices proved crucial for identifying transmission factors and implementing prevention measures. We demonstrated shedding of GAS on settle plates during care of a colonized wound.


PEDIATRICS ◽  
1994 ◽  
Vol 94 (6) ◽  
pp. 1030-1030
Author(s):  
Michael M. Engelgau ◽  
John M. Horan ◽  
Charles H. Woernle ◽  
Banjamin Schwartz ◽  
Richard R. Facklam ◽  
...  

Carriage of the GAS strain was common and widespread following a single fatal case of invasive GAS disease at the child-care center. Risk factors for GAS T-1 carriage did not identify all carriers. Our findings suggest that widespread culturing is needed to identify all potential carriers. The role of prophylactic antibiotic administration in preventing secondary cases could not be determined.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Yu-Tzu Chang ◽  
Chia-Ling Chen ◽  
Chiou-Feng Lin ◽  
Shiou-Ling Lu ◽  
Miao-Huei Cheng ◽  
...  

Group A streptococcus (GAS) imposes a great burden on humans. Efforts to minimize the associated morbidity and mortality represent a critical issue. Glycogen synthase kinase-3β(GSK-3β) is known to regulate inflammatory response in infectious diseases. However, the regulation of GSK-3βin GAS infection is still unknown. The present study investigates the interaction between GSK-3β, NF-κB, and possible related inflammatory mediators in vitro and in a mouse model. The results revealed that GAS could activate NF-κB, followed by an increased expression of inducible nitric oxide synthase (iNOS) and NO production in a murine macrophage cell line. Activation of GSK-3βoccurred after GAS infection, and inhibition of GSK-3βreduced iNOS expression and NO production. Furthermore, GSK-3βinhibitors reduced NF-κB activation and subsequent TNF-αproduction, which indicates that GSK-3βacts upstream of NF-κB in GAS-infected macrophages. Similar to the in vitro findings, administration of GSK-3βinhibitor in an air pouch GAS infection mouse model significantly reduced the level of serum TNF-αand improved the survival rate. The inhibition of GSK-3βto moderate the inflammatory effect might be an alternative therapeutic strategy against GAS infection.


2015 ◽  
Vol 83 (11) ◽  
pp. 4293-4303 ◽  
Author(s):  
Guanghui Liu ◽  
Wenchao Feng ◽  
Dengfeng Li ◽  
Mengyao Liu ◽  
Daniel C. Nelson ◽  
...  

ABSTRACTInvasive M1T1 group AStreptococcus(GAS) can have a mutation in the regulatory system CovRS, and this mutation can render strains hypervirulent. Interestingly, via mechanisms that are not well understood, the host innate immune system's neutrophils select spontaneous M1T1 GAS CovRS hypervirulent mutants, thereby enhancing the pathogen's ability to evade immune killing. It has been reported that the DNase Sda1 is critical for the resistance of M1T1 strain 5448 to killing in human blood and provides pressure forin vivoselection of CovRS mutations. We reexamined the role of Sda1 in the selection of CovRS mutations and in GAS innate immune evasion. Deletion ofsda1or all DNase genes in M1T1 strain MGAS2221 did not alter emergence of CovRS mutants during murine infection. Deletion ofsda1in strain 5448 resulted in Δsda1mutants with (5448 Δsda1M+strain) and without (5448 Δsda1M−strain) M protein production. The 5448 Δsda1M+strain accumulated CovRS mutationsin vivoand resisted killing in the bloodstream, whereas the 5448 Δsda1M−strain lostin vivoselection of CovRS mutations and was sensitive to killing. The deletion ofemmand a spontaneous Mga mutation in MGAS2221 reduced and preventedin vivoselection for CovRS mutants, respectively. Thus, in contrast to previous reports, Sda1 is not critical forin vivoselection of invasive M1T1 CovRS mutants and GAS resistance to innate immune killing mechanisms. In contrast, M protein and other Mga-regulated proteins contribute to thein vivoselection of M1T1 GAS CovRS mutants. These findings advance the understanding of the progression of invasive M1T1 GAS infections.


mBio ◽  
2015 ◽  
Vol 6 (2) ◽  
Author(s):  
Andrew G. Turner ◽  
Cheryl-lynn Y. Ong ◽  
Christine M. Gillen ◽  
Mark R. Davies ◽  
Nicholas P. West ◽  
...  

ABSTRACT Streptococcus pyogenes (group A Streptococcus [GAS]) is an obligate human pathogen responsible for a spectrum of human disease states. Metallobiology of human pathogens is revealing the fundamental role of metals in both nutritional immunity leading to pathogen starvation and metal poisoning of pathogens by innate immune cells. Spy0980 (MntE) is a paralog of the GAS zinc efflux pump CzcD. Through use of an isogenic mntE deletion mutant in the GAS serotype M1T1 strain 5448, we have elucidated that MntE is a manganese-specific efflux pump required for GAS virulence. The 5448ΔmntE mutant had significantly lower survival following infection of human neutrophils than did the 5448 wild type and the complemented mutant (5448ΔmntE::mntE). Manganese homeostasis may provide protection against oxidative stress, explaining the observed ex vivo reduction in virulence. In the presence of manganese and hydrogen peroxide, 5448ΔmntE mutant exhibits significantly lower survival than wild-type 5448 and the complemented mutant. We hypothesize that MntE, by maintaining homeostatic control of cytoplasmic manganese, ensures that the peroxide response repressor PerR is optimally poised to respond to hydrogen peroxide stress. Creation of a 5448ΔmntE-ΔperR double mutant rescued the oxidative stress resistance of the double mutant to wild-type levels in the presence of manganese and hydrogen peroxide. This work elucidates the mechanism for manganese toxicity within GAS and the crucial role of manganese homeostasis in maintaining GAS virulence. IMPORTANCE Manganese is traditionally viewed as a beneficial metal ion to bacteria, and it is also established that most bacteria can tolerate high concentrations of this transition metal. In this work, we show that in group A Streptococcus, mutation of the mntE locus, which encodes a transport protein of the cation diffusion facilitator (CDF) family, results in accumulation of manganese and sensitivity to this transition metal ion. The toxicity of manganese is indirect and is the result of a failure of the PerR regulator to respond to oxidative stress in the presence of high intracellular manganese concentrations. These results highlight the importance of MntE in manganese homeostasis and maintenance of an optimal manganese/iron ratio in GAS and the impact of manganese on resistance to oxidative stress and virulence.


PROTEOMICS ◽  
2007 ◽  
Vol 7 (24) ◽  
pp. 4488-4498 ◽  
Author(s):  
Jason N. Cole ◽  
John A. Aquilina ◽  
Peter G. Hains ◽  
Anna Henningham ◽  
Kadaba S. Sriprakash ◽  
...  

2006 ◽  
Vol 188 (1) ◽  
pp. 77-85 ◽  
Author(s):  
Tracy L. Dalton ◽  
Julie T. Collins ◽  
Timothy C. Barnett ◽  
June R. Scott

ABSTRACT The ability of Streptococcus pyogenes (group A streptococcus [GAS]) to respond to changes in environmental conditions is essential for this gram-positive organism to successfully cause disease in its human host. The two-component system CovRS controls expression of about 15% of the GAS genome either directly or indirectly. In most operons studied, CovR acts as a repressor. We previously linked CovRS to the GAS stress response by showing that the sensor kinase CovS is required to inactivate the response regulator CovR so that GAS can grow under conditions of heat, acid, and salt stress. Here, we sought to identify CovR-repressed genes that are required for growth under stress. To do this, global transcription profiles were analyzed by microarrays following exposure to increased temperature (40°C) and decreased pH (pH 6.0). The CovR regulon in an M type 6 strain of GAS was also examined by global transcriptional analysis. We identified a gene, rscA (regulated by stress and Cov), whose transcription was confirmed to be repressed by CovR and activated by heat and acid. RscA is a member of the MDR1 family of ABC transporters, and we found that it is required for growth of GAS at 40°C but not at pH 6.0. Thus, for GAS to grow at 40°C, CovR repression must be alleviated so that rscA can be transcribed to allow the production of this potential exporter. Possible explanations for the thermoprotective role of RscA in this pathogen are discussed.


2011 ◽  
Vol 193 (23) ◽  
pp. 6539-6551 ◽  
Author(s):  
R. Grifantini ◽  
C. Toukoki ◽  
A. Colaprico ◽  
I. Gryllos

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