What is Staphylococcus Alba?
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Staphylococcus albus (the white Staphylococcus) is spherical bacteria forming clusters. From that characteristic comes the name ( Staphyle - Greek for a bunch of grapes). S albus is the most frequent skin bacteria. It has been considered an innocent partner living on the skin surface of all of us and it has been found in about 30 % of all clean orthopedic operation wounds- all of these wounds healed without complications. This friendly coexistence between the people and the white Staphylococcus changed with the advent of total hip operations. \n\nWhen Staphylococcus albus colonizes the surfaces of total joints, it changes from doctor Jekyll to doctor Hyde. Once fixed to the surface of the total joint prosthesis, S. albus develops a slime cover and changes its characteristics: it develops resistance to antibiotics and causes slow, indolent infections around total joints.\n\nI hope I have been of help.
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See first thing is it causes different effects on human body as per culture, for example.\n\nFastidious gram negative bacilli causes Actinobacillus Opportunistic cause of blood infections.\n------------------------------------------------------\nGram Positive Rods causes.\n1 Bacillus anthracis/cereus/thuringiensis.\n2 anthracis causes anthrax. \n3 Bacillus subtilis. \n4 Lactobacillus. \n\n\nAnd Gram-Positive Cocci causes\n1 Staphylococci form flat packets of cells. Two species are common: \n\nStreptococci cause \n\n"strep throat" \nimpetigo \nmiddle ear infections \nscarlet fever (a result of a toxin produced by the organism) \nrheumatic fever \na rare form of toxic shock syndrome
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Bartonella henselae is a bacterium, which is a prokaryote.  I am not sure what you mean by a "domain", but it is a bacterium that infects cats, dogs, and humans\nIts full taxonomy is:\nBacteria; Proteobacteria; Alphaproteobacteria; Rhizobiales; Bartonellaceae; Bartonella
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Micrococcus are Gram-positive cocci that are 0.5 to 3.5 micrometers in diameter and are usually arranged in tetrads or irregular clusters.\n \nMicrococcus are pigmented bacteria; for example, M. luteus produces yellow colonies when grown on nutrient medium. Micrococcus species are oxidase-positive, which can be used to distinguish them from other bacteria like most Staphylococcus species, which are generally oxidase-negative
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Originally classified in the 1930s as Group D Streptococci, Enterococci were officially given genus status in 1984 after hybridization studies showed a more distant relationship to Streptococci. Enterococci are gram-positive, spherical bacteria that colonize in groups or chains. They are naturally found as part of the digestive tract flora in many organisms, including humans. They are robust microbes able to tolerate relatively high salt and acid concentrations. They also seem to be able to withstand low levels of detergents, explaining why inadequate cleaning procedures can promote Enterococcus infections.\n\nWhat is now recognized as pathogenic Enterococcus was studied as early as the late 1900s. Currently, Enterococcus infections account for 12% of all nosocomial infections, second only to E. coli. An Enterococcus infection can cause complicated abdominal infections, skin and skin structure infections, urinary tract infections and infections of the blood stream. These infections can be difficult to treat, particularly in cases where the strain involved has developed resistance to several antibiotics. Infection can be life threatening in such instances, especially if the patient is already immunodeficient. \n\nThere are two species of Enterococci which cause the symptoms described above, E. faecalis, which accounts for the majority of infections (79%), and E. faecium. In a study conducted between 1995 and 1997, data were collected from over 15,000 Enterococcus isolates. Of those, less than 2% of E. faecalis were found to be resistant to ampicillin and vancomycin, whereas 83% of the E. faecium isolates were resistant to ampicillin and 52% were resistant to vancomycin. \n\nE. faecium is known to have a resistance to several types of antibiotics including quinolones and aminoglycosides. Resistance to penicillin was first observed in E. faecium in 1983, and in 1988 the first cases of resistance to the "antibiotic of last resort", vancomycin, were detected in Europe. Vancomycin-resistant strains of E. faecium were reported in the US in 1989. Resistance to several antibiotics and tolerance for adverse conditions makes E. faecium a major concern for the medical community, which has dubbed this microbe a "supergerm".
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Do you mean Leptothrix?\n \nLeptothrix is a bacteria occasionally found in large numbers in the vagina and cervix. It apparently causes no harm and is not considered a pathogen. It would not be worth noting except for two characteristics; It can live comfortably with Trichomonas and it can resemble yeast on a wet mount. It may safely be ignored.
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INTRODUCTION — Shortly after the introduction of methicillin in 1959, outbreaks of methicillin-resistant Staphylococcus aureus (MRSA) infections were reported in the early 1960s [1]. Methicillin resistance in S. aureus is defined as an oxacillin minimum inhibitory concentration (MIC) 4 µg/mL. Isolates resistant to oxacillin or methicillin are also resistant to all beta-lactam agents including cephalosporins.\n\nMethicillin resistance is mediated by the mecA gene, which encodes for an abnormal low-affinity binding protein, PBP-2a that permits the organism to grow and divide in the presence of methicillin and other beta-lactam antibiotics. (See "Mechanisms of antibiotic resistance in Staphylococcus aureus").\n\nThe evidence suggests that a single clone of MRSA accounted for most of the isolates recovered during the 1960s [2,3] and that five major MRSA clones had emerged worldwide by 2002 [4]. Dissemination of resistance was mediated by horizontal transfer of the mecA gene and related regulatory sequences [5]. Since that time, MRSA has increased in prevalence worldwide as both a nosocomial and, more recently, a community-associated pathogen.\n\nThe epidemiology and clinical manifestations of MRSA infection in adults will be reviewed here. The prevention and control and the treatment of MRSA infections in adults is discussed separately. (See "Prevention and control of methicillin-resistant Staphylococcus aureus" and see "Treatment of methicillin-resistant or vancomycin resistant Staphylococcus aureus infection in adults").\n\nEPIDEMIOLOGY — MRSA was at first primarily a healthcare-associated (nosocomial) infection, with only small numbers of community-associated cases [4]. However, it is now an increasingly prevalent community-associated pathogen. Such patients acquire MRSA infection in the outpatient setting, and are infected at the time of hospital admission.\n\nCommunity-associated (CA) MRSA isolates usually have different molecular and antimicrobial susceptibility characteristics from healthcare-associated (HA) MRSA. However, nosocomially acquired MRSA can spread to household and community contacts and be a source of community-associated infection [6]. In addition, CA-MRSA is emerging as a significant cause of nosocomial infection as illustrated by analysis of 132 cases of MRSA blood stream infection in patients collected at an urban public hospital in 2004 [7]. Molecular typing studies demonstrated that 39 of 116 isolates (34 percent) were MRSA USA300 genotype, the predominant cause of CA-MRSA infection in the area.\n\nGenetics of methicillin resistance — Molecular typing techniques have provided insights into the epidemiology of MRSA and to differences between HA-MRSA and CA-MRSA. The genetic determinants of antibiotic resistance in MRSA are discussed in detail separately, but will be reviewed briefly here. (See "Mechanisms of antibiotic resistance in Staphylococcus aureus").\n\nThe mecA gene responsible for methicillin resistance is located on a mobile genetic element called staphylococcal cassette chromosome (SCCmec). Sequencing SCCmec from many MRSA strains has revealed that there are five SCCmec types (I-V) that vary in genetic makeup and size. Transfer of SCCmec from MRSA into well-adapted strains of methicillin-susceptible S. aureus (MSSA) has occurred on a number of occasions, resulting in new MRSA strains that spread rapidly in healthcare institutions. A majority of HA-MRSA clones have type I, II, or III SCCmec and are multidrug resistant [8].\n\nIn contrast, a majority of CA-MRSA strains have type IV SCCmec [9-11]. Because type IV SCCmec does not carry the multiple antibiotic resistance genes common among types I to III [10,11], CA-MRSA are usually resistant only to methicillin, other beta-lactam antibiotics, and erythromycin, but are usually susceptible to other classes of antibiotics, particularly trimethoprim-sulfamethoxazole and clindamycin [10,12-16]. CA-MRSA in so
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Those answsers are wrong. It is a bacteria that lives on an aphid. Here is the link to prove it:\n\nhttp://phylogenomics.blogspot.com/2006/10/worlds-smallest-genome-of-cellular.html
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Effective treatment must include removal and control of Staphylococcus bacteria.  Antibacterial Cleanser kills propionibacterium acnes, and it also kills Staphylococcus (staph), E. coli, Salmonella and a number of other dreaded bacteria.  This is achieved with cinnamon bark extract and a combination of herbs with unique antibacterial properties.  Antibacterial Cleanser will remove staph from the skin to help prevent new infections and kill bacteria in existing infection, which spill onto the skin.
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Staph is a very dangerous infection that can be life threatening. I had a staph infection after a hysterectomy and almost died from it.  I was in the hospital 8 days on multiple IV antibiotics, and my doctor told me later he wasn't too sure I was going to make it.  My sister-in-law's father died from one that got into his system through a cut in the skin. The infection can migrate to various areas of the body and be very difficult to find and treat. It's nothing to mess around with.
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http://www.microbesonline.org/operons/gnc205922.html
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it's MRSA -- methcillin resistant staph aureus -- it's a bacterial infection that is resistant to one of the most potent anti-biotic, methcillin. you have to be hospitalized for this, but there is a cure. doctors now are using Vancomycin - IV for treatment of MRSA.
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It is described as a gram-negative, encapsulated, facultative anaerobic, non-spore forming, nonmotile pleomorphic coccobacillus.\n\npleomorphic - Occurring in various distinct forms. In terms of cells, having variation in the size and shape of cells or their nuclei. \n\ncocobacillus- Ovoid
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http://www.link.med.ed.ac.uk/ridu/Mrsa.htm
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Agrobacterium is a genus of bacteria that causes tumors in plants. Agrobacterium tumefaciens is the most commonly studied species in this genus. Agrobacterium is well known for its ability to transfer DNA between itself and plants, and for this reason it has become an important tool for plant improvement by genetic engineering.\n\n\nA. tumefaciens causes crown-gall disease in plants. The disease is characterised by a tumour like growth or gall on the infected plant, often at the junction between the root and the shoot. Tumors are incited by the transfer of a DNA (T-DNA) segment from the bacterial tumour-inducing (Ti) plasmid. The closely related species, A. rhizogenes, induces root tumors, and carries the distinct Ri (root-inducing) plasmid. Although the taxonomy of Agrobacterium is currently confused it can be generalised that 3 biovars exist within the genus, A. tumefaciens or biovar 1, A. rhizogenes or biovar 2, and A. vitis or biovar 3. Strains within biovars 1 and 2 are known to be able to harbour either a Ti or Ri-plasmid, whilst strains of biovar 3, generally restricted to grapevines, can harbour a Ti-plasmid. Non-Agrobacterium strains have been isolated from environmental samples which harbour a Ri-plasmid whilst laboratory studies have shown that non-Agrobacterium strains can also harbour a Ti-plasmid. Many environmental strains of Agrobacterium do not possess either a Ti or Ri-plasmid. These strains are avirulent.\n\nThe plasmid T-DNA is incorporated into the genome of the host cell by homologous recombination, and the virulence (vir) genes on the T-DNA are expressed, causing the formation of a gall. The T-DNA carries genes for the biosynthetic enzymes for the production of unusual amino acids, typically octopine or nopaline. It also carries genes for the biosyntheis of the plant hormones, auxin and cytokinins. By altering the hormone balance in the plant cell, the division of those cells cannot be controlled by the plant, and tumors form. The ratio of auxin to cytokinin produced by the tumor genes determines the morphology of the tumor (root-like, disorganized or shoot-like).\n\n[edit]\nAgrobacterium in biotechnology\nThe ability of Agrobacterium to transfer genes to plants has been exploited for genetic engineering for plant improvement. A modified Ti or Ri plasmid can be used. The plasmid is 'disarmed' by deletion of the tumor inducing genes, the only essential parts of the T-DNA are its two small (25 base pair) border repeats, at least one of which is needed for plant transformation. A team of researchers led by Dr Mary-Dell Chilton were the first to demonstrate that the virulence genes could be removed without adversely affecting the ability of Agrobacterium to insert its own DNA into the plant genome (1983).\n\nThe genes to be introduced into the plant are cloned into the T-DNA region of the disarmed plasmid, together with a selectable marker (such as antibiotic resistance) to enable selection for plants that have been successfully transformed. Plants are grown on media containing antibiotic following transformation, and those that do not have the T-DNA integrated into their genome will die.\n\nTransformation with Agrobacterium can be achieved in two ways. Protoplasts, or leaf-discs can be incubated with the Agrobacterium and whole plants regenerated using plant tissue culture. A common transformation protocol for Arabidopsis is the floral-dip method: the flowers are dipped in an Agrobacterium culture, and the bacterium transforms the germline cells that make the female gametes. The seeds can then be screened for antibiotic resistance, and plants that have not integrated the plasmid DNA will die.\n\nAgrobacterium does not infect all plant species, but there are several other effective techniques for plant transformation including the gene gun.
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Methicillin-resistant Staphylococcus aureus (MRSA) is a specific strain of the Staphylococcus aureus bacterium that has developed antibiotic resistance to all penicillins, including methicillin and other narrow-spectrum β-lactamase-resistant penicillin antibiotics.[1] MRSA was first discovered in the UK in 1961 and is now widespread, particularly in the hospital setting where it is commonly termed a superbug.\n\nMRSA may also be known as oxacillin-resistant Staphylococcus aureus (ORSA) and multiple-resistant Staphylococcus aureus, while non-methicillin resistant strains of S. aureus are sometimes called methicillin-susceptible Staphylococcus aureus (MSSA) if an explicit distinction must be made.\n\nAlthough MRSA has traditionally been seen as a hospital-associated infection, there is currently an epidemic of community-acquired MRSA in the USA. The abbreviations CA-MRSA (community-associated MRSA) and HA-MRSA (hospital-associated MRSA) are now commonly seen in the literature.\n\nStaphylococcus bacteria are extremely common in the environment (and a third of humans world-wide are estimated to carry it on their bodies and are not harmed by it), and is usually not a problem to healthy individuals. Historically, staph infections begin only after the individual has suffered a skin break or open wound. Recently, due to institutional overuse of antibiotics, strains of staphylococcus aureus have developed drug resistance. If an individual has a weak immune response to the bacteria, a MRSA infection can result even with no apparent open wound. The symptoms can range from skin boils to necrotizing fasciitis, popularly known as flesh-eating disease. MRSA infections are typically combatted with vancomycin, however, vancomycin-resistant staphylococcus has recently appeared.\n\nAlthough Noskin and others report that a patient infected with MRSA is five times more likely to die than other patients; it is not clear that patients who are infected with MRSA have an increased death rate. Wyllie et al. report a death rate of 34 percent within 30 days among patients infected with MRSA, while among MSSA patients the death rate was similar at 27%\n\nVancomycin and teicoplanin are glycopeptide antibiotics used to treat MRSA infections. Teicoplanin is a structural congener of vancomycin that has a similar activity spectrum but a longer half-life (t½). Both drugs have low oral absorption and must therefore be administered intravenously for systemic infections. One of the problems with vancomycin is not just that its route of administration is inconvenient, but also that it is inferior in terms of its efficacy compared to antistaphylococcal penicillins.\n\nSeveral new strains of MRSA have been found showing antibiotic resistance even to vancomycin and teicoplanin; those new evolutions of the MRSA bacteria are dubbed vancomycin intermediate-resistant Staphylococcus aureus (VISA). Linezolid, quinupristin/dalfopristin, daptomycin, tigecycline are more recent additions to the therapeutic arsenal, generally reserved for severe infections which do not respond to glycopeptides. Less severe infections may be treated by oral agents including: linezolid, rifampicin+fusidic acid, pristinamycin, co-trimoxazole (trimethoprim+sulfamethoxazole), doxycycline, and clindamycin.
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MRSA, Methicillin Resistant Staphylococcus Aureus, is a bacteria infection that is resistant to certain antibiotics. The organism, Staphylococcus aureus, is found normally on many individuals skin and seems to cause no major problems.  The problems start when that bacteria finds its way into the body.  \n\nMRSA infections can cause a broad range of symptoms depending on the part of the body that is infected. These may include surgical wounds, burns, catheter sites, eye, skin and blood. Infection often results in redness, swelling and tenderness at the site of infection. Sometimes, people may carry MRSA without having any symptoms.\n\nSome people can carry MRSA for days to many months, even after their infection has been treated.  It is usually treated with an antibiotic called vancomycin.\n\nCareful hand washing is the single most effective way to control spread of MRSA.  If basic hygiene precautions are followed, MRSA carriers are not a hazard to others including their family and friends.\n\nHere is a site that can tell you more about it than there is room to post here: \nhttp://www.mrsaresources.com/