streptococcus where they also tried mitomycin treatment to induce phage indicible island

What was the first Streptococcus phage discovered?

Identification of prophages induced by mitomycin C treatment. To determine which of the prophages were induced by treatment of strain MGAS315 with mitomycin C, we conducted PCR with purified phage DNA template and primers specific for each of the six virulence factor genes carried by the prophages in this strain (Table (Table1). 1).

Does Streptococcus mitis induce disease in neutropenic mice?

Mar 20, 2001 · Researchers at The Rockefeller University have discovered a powerful new way to destroy on contact the bacteria that cause strep throat, flesh-eating disease and a variety of other infections. The ...

Which lysin mediates the binding of Streptococcus mitis to human platelets?

Oct 01, 2002 · Streptococcus pyogenes, one of the most common human bacterial pathogens, has evolved diverse mechanisms that allow the bacteria to evade the immune system and cause disease 1.The molecular bases ...

What is the host range of Streptococcus phage 1?

Streptococcus is a genus of gram-positive coccus (plural cocci) or spherical bacteria that belongs to the family Streptococcaceae, within the order Lactobacillales (lactic acid bacteria), in the phylum Bacillota. Cell division in streptococci occurs along a single axis, so as they grow, they tend to form pairs or chains that may appear bent or twisted.. This differs from staphylococci, …

Is the Streptococcus phage A bacteriophage?

What media is used for Streptococcus?

How can I induce my phages?

What is the name of the toxin that the bacteriophage codes for scarlet fever?

Where is Streptococcus found?

Where do Streptococcus bacteria live?

What is lysogenic induction?

What is induction microbiology?

How does lysogeny provide immunity against further infection?

What is another word for bacteriophage?

What toxin does Streptococcus pyogenes release?

What is phage encoded?

What is the name of the group of bacteria that causes infections in the oropharynx?

Viridans group streptococci (VGS), a genetically heterogeneous group of bacteria, are the predominant bacteria in the human oropharynx ( 1 ). VGS cause a wide range of infections in humans, including bacteremia in patients with neutropenia, infective endocarditis, and orbital cellulitis ( 2 – 5 ). However, despite the substantial clinical effect ...

Is S. mitis a VGS?

Indeed, a recent microbiome study showed that S. mitis is the predominant VGS species isolated from buccal mucosa samples from healthy persons ( 1 ). However, in our study, S. mitis not only caused the majority of neutropenic infections but also caused a disproportionate percentage of serious infections ( Figure 2 ).

Is VGS an infectious agent?

The emergence of VGS as common infectious agents has coincided with the increasing use of prophylactic antimicrobial drugs, especially fluoroquinolones, for patients with neutropenia ( 36 ). However, despite the clear clinical consequences of VGS infections, there is minimal understanding of their pathophysiology.

Is VGS a pathogen?

Since first being identified as causative agents of infections in cancer patients with neutropenia ≈35 years ago ( 33 ), VGS have come to be appreciated as major bacterial pathogens in patients with malignancy ( 2, 12, 14, 34, 35 ). The emergence of VGS as common infectious agents has coincided with the increasing use of prophylactic antimicrobial drugs, especially fluoroquinolones, for patients with neutropenia ( 36 ). However, despite the clear clinical consequences of VGS infections, there is minimal understanding of their pathophysiology.

What university discovered the new way to destroy on contact the bacteria that cause strep throat?

Rockefeller University. Summary: Researchers at The Rockefeller University have discovered a powerful new way to destroy on contact the bacteria that cause strep throat, flesh-eating disease and a variety of other infections. The technique, which may not cause the bacteria to evolve resistant strains as antibiotics do, ...

Why is it important to control streptococci?

Controlling streptococci in the population would lessen the chance of someone being exposed to strep throat, which would reduce cases of rheumatic fever. After phages were discovered in 1917, researchers initially thought they would provide an effective way to kill bacteria.

What is the new way to destroy bacteria?

The technique, which may not cause the bacteria to evolve resistant strains as antibiotics do , also could have applications for many other bacterial diseases.

Who is the professor of bacterial biology who uses enzymes to kill bacteria?

Rockefeller University Professor Vincent Fischetti, Ph.D. , who led the research, employs these same enzymes to attack the bacteria, Group A streptococci, from the outside. The effect is remarkable. "It kills the target bacteria instantly.

Can strep throat cause rheumatic fever?

Although not life-threatening in itself, strep throat can develop into rheumatic fever, which permanently damages the heart. At any one time, up to one-fifth of the population carries group A strep in their throats, and each year 30 percent of children develop strep throat infections.

Why do new recruits get penicillin?

At present, all new recruits receive a penicillin injection to prevent strep outbreaks that inevitably occur in a group of people sharing close quarters. Antibiotic resistance compelled the military to try shifting away from such routine use of the drug.

When were phages discovered?

After phages were discovered in 1917 , researchers initially thought they would provide an effective way to kill bacteria. They soon learned, however, that phages must bind to specific receptors on the surface of bacteria before injecting their DNA; as bacteria evolve, they change their receptors and shut out the phages.

Competing interests

The authors are funded by Hansa Medical AB. Hansa Medical has filed a patent application on IdeS. The application is pending.

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What are the most important groups of streptococci?

In the medical setting, the most important groups are the alpha-hemolytic streptococci S. pneumoniae and Streptococcus viridans group, and the beta-hemolytic streptococci of Lance field groups A and B (also known as “group A strep” and “group B strep”).

What are the two main clades of Streptococcus?

The results revealed the presence of two main clades at the highest level within Streptococcus, termed the “Mitis-Suis” and “Pygogenes-Equinus-Mutans” clades. The “Mitis-Suis” main clade comprises the Suis subclade and the Mitis clade, which encompasses the Angiosus, Pneumoniae, Gordonii and Parasanguinis subclades.

What is the genus of streptococcus?

Species. Streptococcus is a genus of gram-positive coccus (plural cocci) or spherical bacteria that belongs to the family Streptococcaceae, within the order Lactobacillales (lactic acid bacteria), in the phylum Firmicutes.

What is the cytotoxin that is secreted by most group A Streptococcus?

Streptolysin O is an oxygen-sensitive cytotoxin, secreted by most group A Streptococcus (GAS), and interacts with cholesterol in the membrane of eukaryotic cells (mainly red and white blood cells, macrophages, and platelets), and usually results in beta-hemolysis under the surface of blood agar.

Is Streptococcus dysgalactiae a GGS?

Streptococcus dysgalactiae is the predominant species encountered, particularly in human disease. S. canis is an example of a GGS which is typically found on animals, but can cause infection in humans. S. phocae is a GGS subspecies that has been found in marine mammals and marine fish species.

How many subclades are there in Streptococcus?

In total, 14 distinct subclades have been identified within the genus Streptococcus, each supported by reliable branching patterns in phylogenetic trees and by the presence of multiple conserved signature indels in different proteins that are distinctive characteristics of the members of these 14 clades.

How many proteins are in the Streptococcus genome?

Most Streptococcus genomes are 1.8 to 2.3 Mb in size and encode 1,700 to 2,300 proteins. Some important genomes are listed in the table. The four species shown in the table ( S. pyogenes, S. agalactiae, S. pneumoniae, and S. mutans) have an average pairwise protein sequence identity of about 70%. feature.

What is the name of the gram positive bacterium that causes dermatitis?

Streptococcus pyogenes (group A Streptococcus) is a gram-positive bacterium that causes several diseases in humans. S. pyogenes usually colonizes the throat or skin epithelial surfaces and causes a wide variety of clinical manifestations, such as noninvasive pharyngitis, dermatitis, and scarlet fever ( 1,2 ).

Can S. pyogenes be isolated from dogs?

We know of no other reports of isolation of this microorganism from animals.

Is S. pyogenes a human disease?

S. pyogenes is a human pathogen that has rarely been isolated from animals. It has been isolated from abscesses in cervical and mesenteric lymph nodes and liver of a free-living European hedgehog ( E. europaeus) and from 2 dogs with severe colonic disease and conjunctivitis ( 5–7 ).

How many deaths are caused by streptococcus pyogenes?

Streptococcus pyogenes is a significant human pathogen, annually causing over 700,000,000 infections and 500,000 deaths ( Carapetis et al., 2005 ). Genome sequencing has revealed that prophages and other mobile genetic elements are important features of Streptococcus pyogenes (group A streptococcus) chromosomes, sometimes contributing up to 10% of the total DNA ( Desiere et al., 2001; Ferretti et al., 2001; Banks et al., 2002; Canchaya et al., 2002 ). These genome prophages follow a typical lambdoid gene arrangement, with sequentially organized modules for integration and lysogeny, DNA replication, transcriptional regulation, DNA packaging and head assembly, tail and tail fiber assembly, and lysis ( Desiere et al., 2001; Banks et al., 2002; Canchaya et al., 2002; Brussow et al., 2004 ). In S. pyogenes and many other pathogens, these essential phage genes are often followed by one or more virulence genes such as toxins ( Brussow et al., 2004 ). Numerous genes on S. pyogenes chromosomes are the targets for site-specific integration by these mobile genetic elements, and for some of these genes, integration has the potential to interrupt or alter their transcription ( McShan and Ferretti, 2007 ). Of these targeted genes, one location stands out both for its frequency of occupation by a chromosomal island (CI) as well as the potential phenotypic impact integration would have on the cell: the operon encoding the genes for DNA mismatch repair (MMR). We have characterized phage-like CI in S. pyogenes that integrate into MMR gene mutL, silencing this gene and the other downstream genes of the operon ( Scott et al., 2008, 2012 ). The integration of the S. pyogenes Chromosomal Island M1 (SpyCIM1) into the chromosome induces a complex mutator phenotype that results from the interruption of the operon and downstream DNA repair genes ( Scott et al., 2008, 2012 ). Largely due to the extensive and ongoing efforts to sequence the genomes of many species of bacteria, additional islands integrated into mutL also have been identified in other Streptococcus species. This review will examine the CI identified so far, their known or potential impacts on host phenotype and survival, and implications for the evolution of this group and their host bacteria. A note concerning nomenclature: when referred to collectively as a group, S. pyogenes phage-like CI are referred to as SpyCI, but a specific CI is identified so to associated it with a particular strain or isolate (e.g., SpyCIM1, SpyCIM49, etc.). The same convention is applied to CI from other streptococcal species.

What is the origin of SpyCI?

SpyCI and other phage-like chromosomal islands may have originated from defective prophages, but their biology suggests an even more complex origin. The defining gene of SpyCI is the integrase ( int ), whose expression and regulation controls the molecular switch for the MMR operon. Within the known SpyCI, int is highly conserved at both the gene and protein level ( Scott et al., 2008, 2012 ). The SpyCI integrase genes form a distinct group within the S. pyogenes prophage integrases ( McShan, 2005 ), although the integrase encoded by S. pyogenes strain NZ131 prophage NZ131.1 is 62% identical to the SpyCIM1 integrase at the amino acid level, suggesting that these genes may have had a recent common origin ( McShan et al., 2008 ). The integration site for prophage NZ131.1 is near the promoter of hypothetical protein Spy49_0371 ( McShan et al., 2008 ), which is unrelated to the MMR operon.

What is site specific recombination?

Typically, site-specific recombination occurs between bacterial and phage genomes such that the transcription of the targeted host gene is unimpeded by the presence of the prophage ( Fouts, 2006 ). This maintenance of gene function is accomplished by two factors: (1) duplication of the host DNA sequence at the site of crossover by a portion of the phage DNA and (2) integration at the 3′ end of the targeted gene so that the duplication can complete the original bacterial ORF ( Fouts, 2006; Louie et al., 2007; McShan and Ferretti, 2007 ). By contrast, integration into the 5′ end or the middle of a gene could result in the disruption of normal transcription with a concomitant loss of gene function. Occasional examples of prophages altering the expression of host genes have been reported in Escherichia coli and Staphylococcus aureus ( Mason and Allen, 1975; Lee and Iandolo, 1986; Thomas and Drabble, 1986; Coleman et al., 1991; Campbell et al., 1992 ), but these occurrences have been notable in part because of their rarity. By contrast, genome sequencing has revealed that S. pyogenes prophages frequently target attachment sites positioned at the promoter or 5′ end of genes that, following integration, potentially could alter gene expression, or create polar mutations ( McShan and Ferretti, 2007 ). Of these mobile genetic elements with the potential to alter gene expression, the phage-like chromosomal island that frequently targets and regulates the DNA mismatch repair (MMR) operon of S. pyogenes is perhaps the most remarkable.

Is Streptococcus pyogenes a pathogen?

Streptococcus pyogenes belongs to the serological group A among the streptococci (group A Streptococcus, GAS) and is an exclusively human pathogen. GAS causes significant disease worldwide and adds a large burden to national health care systems ( Tan et al., 2014 ). An excellent compilation of data and estimates of the global burden of GAS diseases from 2005 revealed 616 million cases of pharyngitis, 111 million cases of pyoderma and at least 517,000 deaths due to severe invasive diseases and sequelae. This dataset is manifesting the important status of GAS among bacterial pathogens and is an impressive documentation of GAS impact on global mortality and morbidity ( Bisno et al., 2005; Carapetis et al., 2005; Ralph and Carapetis, 2013 ).

Can antibiotics be used to treat GAS biofilms?

The standard antibiotic medication for patients with GAS infections is not sufficient to eradicate GAS biofilms . Alternative or additional therapeutics are currently investigated. Phage lysin C represents the most promising candidate for clinical application. However, more efforts are needed in developing treatment strategies to prevent extensive and repeated antibiotic treatment in patients with biofilm associated recurrent GAS infections.

What are the human interactions with humans?

Interactions with humans range from asymptomatic carriage over mild and superficial infections of skin and mucosal membranes up to systemic purulent toxic-invasive disease manifestations. Particularly the latter are a severe threat for predisposed patients and lead to significant death tolls worldwide.

Can secreted proteins impair biofilm formation?

From all studies introduced above the M protein as one major virulence determinant of GAS seems to support biofilm formation, but secreted proteins and capsule could impair biofilm formation. However, it has to be kept in mind that the data discussed here are all based on in vitro experiments that most likely only poorly resemble the in vivo situation. Most of the experimental data are based on biofilms formed on abiotic plastic surfaces, sometimes coated with matrix or serum proteins. Only few studies analyzed biofilms grown on epithelial cells ( Fiedler et al., 2013; Marks et al., 2014 ). To our knowledge, device-associated GAS biofilms have never been described in patients. Furthermore, although GAS microcolony formation in the oropharynx has been observed ( Diaz et al., 2011; Roberts et al., 2012; Torretta et al., 2012; Woo et al., 2012 ), it is yet not known whether complex biofilms—as they can be obtained in vitro —are actually occurring in patients. Therefore, taken together, the relevance of these in vitro data for real infections in patients remains unclear.

Can a GAS survive antibiotics?

Hence, GAS organized in biofilm structures are able to survive antibiotic treatment that is adequate for planktonic GAS. To reach a better clinical outcome and lower treatment failure rates, it would be necessary to adapt treatment of GAS infections to achieve an effective degradation of biofilm structure.

Is a GAS a human pathogen?

GAS was considered a classical extracellular human pathogen for a long time . Numerous studies have evaluated the potential of these bacteria to adhere to and internalize into almost all host cell types, a feature which was discussed as reason for the occurrence of recurrent GAS infections ( Facinelli et al., 2001; Podbielski and Kreikemeyer, 2001 ). However, now it is under debate if recurrence is sufficiently explained by GAS host cell adherence/internalization or if GAS biofilms play a so far underappreciated role. Moreover, the question if GAS biofilms are clinically relevant needs to be addressed. Here we discuss this aspect with a careful look on terminology (microcolony vs. biofilm) and in vitro vs. in vivo observations and studies.

What is the B streptococci?

Group B streptococci cause a narrow band of beta-hemolysis on blood agar plates. They are distinguished from other streptococci because of their ability to hydrolyze hippurate. Although they can cause disease in other groups, they are most commonly associated with infections of the newborn. Newborns are at particular risk of Group B sepsis or meningitis if their mother is vaginally colonized with Gp B streptococcus, lacks type-specific antibody, and there is prolonged ruptured membranes. These infections are life-threatening and can also result in permanent disability to the infant. Chemoprophylaxis with penicillin is recommended for all pregnant women who are colonized or are at high risk.

How many species are in the streptococci?

This is a heterogeneous group of streptococci that includes 24 different species. They were originally grouped on the basis of the alpha hemolysis that is present (for the most part) when they are grown on blood agar plates. They are part of the oropharyngeal flora and some species can also be found in the gastrointestinal tract. They are relatively avirulent organisms however they do cause dental caries (S. mutans) and are the most common cause of subacute infective endocarditis.

Is streptococci a heterogeneous group?

The genus Strepto coccus includes a heterogeneous group of different Gram positive species (>30) that are identified on Gram stain by their spherical or ovoid shape and their tendency to grow in pairs and chains. They are nonmotile, non-spore forming, and mostly facultatively anaerobic. Streptococci are a heterogeneous group that includes a variety of species capable of causing a diverse array of different diseases ranging from minor soft tissue infections to life-threatening sepsis. The most important pathogens in this group are Streptococcus pyogenes (group A streptococcus), Streptococcus agalactiae (group B streptococcus) and Streptococcus pneumoniae (pneumococcus). DNA homology studies have established Enterococcus (formerly streptococci) as a separate genus, distinct from Streptococcus. This lecture will cover only two of these pathogens, S. pyogenes and S. pneumoniae. Although not covered in the lecture you are also responsible for S. agalactiae, enterococci and viridans streptococci.

What is the most common bacterial infection of the throat in children?

Pharyngitis. GAS are the most common bacterial infection of the throat in children, especially ages 5-15. They appear capable of causing infections at this site because of the ability of GAS to adhere to and perhaps be internalized by oropharyngeal epithelial cells. This occurs via specific adhesin – receptor interactions (some are noted above).

When was pneumococci first discovered?

The pneumococcus was first recognized in the 1880’s in France by Pasteur and by Sternberg in the United States. This pathogen continues to be the most commonly identified cause of bacterial pneumonia and is among the most common causes of mortality worldwide (3-5 million deaths/year). With the widespread development of multidrug-resistant pneumococci in South Africa in the late 1970’s therapy of these infections has become increasingly problematic.

Why are streptococci white?

Formerly classified as streptococci, DNA analysis has resulted in the separation of these Gram positives into their own species. They grow as white colonies on blood agar plates and are generally nonhemolytic (gamma hemolysis). They are part of the normal gastrointestinal flora in part because of their resistance to bile salts. They are relatively common causes of infective endocarditis and have emerged, in part due to their increasing resistance to many antimicrobials, as important nosocomial pathogens.

What are the enzymes produced by gas?

Enzymes produced by GAS. Streptolysins O and S are responsible for the hemolysis seen on blood agar plates. Their role as virulence determinants has not been established. Other enzymes, including DNases, hyaluronidases and streptokinase may contribute to tissue breakdown and pus formation. Antibodies to these enzymes have also been used to diagnose recent streptococcal infections.

Introduction

• The study cohort comprised patients at MD Anderson Cancer (MDACC) who had VGS isolated from their blood between July 1, 2011, and December 1, 2012. MDAAC is a 600-bed referral cancer hospital in Houston, Texas, USA. We used a standardized data collection form to abstract clinical data from the comprehensive electronic medical records of patients wi...

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