Who first discovered Staphylococcus Aureus?

Answer 1

Rosenbach in 1884

Answer 2

RE:
Who first discovered Staphylococcus Aureus?

Answer 3

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.

MRSA 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.

Answer 4

Staphylococci were first observed in human pyogenic lesions by von Recklinghausen
Pasteur obtained the liquid cultures of the cocci from pus
The name Staphylococcus was given by Sir Alexander Ogston
But, Rosenbach gave the name Staph aureus and Staph albus

sO your answer is Rosenbach

Answer 5

I wouldnt say its related to a sexually transmitted disease, but staph is on the the organisms that is naturally occuring bacteria on our skin all the time. If you had sex and it was on you or your partners skin, it is possible for the bacteria to cause an infection during sexual intercourse. Expecially if you had kind of "rough" sex and may have made yourself raw. I can see that happening. The vagina is not sterile so there are jerms there. Our body keeps this natural bacteria (flora) to fight off other forms of infection, sometimes thats why we get infections.

Answer 6

Staphylococci are spherical, gram positive bacteria of the micrococcaceae family. They are found primarily on the skin and in the mucous membranes of humans and other warm-blooded animals, and aggregate into small, grape-like clumps (8). Staphylococci-related infections are one of the most common causes of nosocomial (hospital-acquired) infections, yet they are increasingly difficult to treat due to the rate at which the bacteria acquire antibiotic resistance.

Ninety percent of Staphylococci strains are penicillin resistant --- leaving only methicillin and vancomycin to treat the majority of infections. However, with increasing numbers of reports of methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococci (VRE) chemists are faced with the daunting task of generating new antibiotics with novel modes of action, and doctors with the task of curing seemingly incurable infections.

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Basic Facts

The genome of Staphylococcus aureus N35.(7)

The Staphylococcus genus is divided into two groups: the aureus and non-aureus Staphylococci. The two types are distnguished from each other, traditionally, by their coagulase activity. S. aureus staphylococci are the only variety that test positive in the coagulase test (they maintain the ability to clot blood plasma).

Staphylococcus can cause skin, heart valve, blood, and bone infections, which can lead to septic shock and death. These infections are primarily caused by the toxins which Staphylococci produce. For example, the enterotoxins produced by S. aureus are a significant cause of food poisoning (2) and the superantigens can cause toxic shock syndrome if present in the blood stream (9). In their more potent forms, the toxins are responsible for damaging host tissues, inhibiting phagocytosis (whereby the host neutralizes the Staphylococci toxins and eliminates the bacteria), and causing disease symptoms (8).

Ninety percent of Staphylococcus strains are resistant to penicillin and penicillin-derived antibiotiocs. The next line of attack, methicillin, is increasingly becoming less effective: between 1975 and 1991, the prevalence of methicillin-resistant strains of S. aureus increased ~26% (13). While non-hospital acquired Staphylococcus infections can be treated with penicillin-derived antibiotics, hospital-acquired infections are entirely resistant to penicillin and require more aggressive antibiotic treatments.

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S. aureus
S. aureus is one of the major causes of hospital-acquired infection. One study ranked it fourth in a listing of the “Pathogens Most Frequently Isolated From Hospitalized Patients When All Anatomic Sites Are Considered” (3). Approximately 40% of the general population and 50 – 90% of health care practitioners harbor an S. aureus colony in their anterior nasal passage. Infection becomes a problem when bacteria migrate from their normal habitat, especially in individuals already suffering from a compromised immunologic response.

S. aureus most commonly causes a localized skin infection, although it can also infect the eye, nose, throat, urethra, vagina, and gastrointestinal tract. In addition, S. aureus can cause more serious ailments when it enters the bloodstream, such as pneumonia, osteomyelitis, arthritism endocarditis, myocarditis, brain abscesses and meningitis (5). (See inset on S. aureus virulence factors and toxins)

The toxins most relevant to disease causing symptoms in humans are the superantigens and a-toxins. The a-toxins oligomerize to form pores in the host cellular membrane, allowing cellular contents to leak into the extracellular matrix. The superantigens, consisting of enterotoxins and the toxic shock syndrome toxin, are responsible for S. aureus-related food poisoning and toxic shock syndrome, respectively. (See insets on “How do Superantigens work?" and "How do Alpha Toxins Work?") Individuals with damaged or severely compromised immune systems, such as recent surgical recoveries or burn victims, IV drug users, insulin-dependent diabetics and hemodialysis patients are more susceptible to Staphylococcus infection than healthy individuals. Individuals identified with Staphylococcus infections are most commonly found in hospital intensive care units, burn units, and dermatology and surgical units, reflecting the increased susceptibility of these individuals to Staphylococcus infections due to compromised immune function (1). Treatment of S. aureus infections showing no signs of broad-antibiotic resistance is achieved with a cocktail of antibiotics, including some of the following: flucloxacillin, gentamycin, rifamicin, fusidic acid, erythromycin, vancomyin, and cefotaxime. However, 90% of S. aureus strains are penicillin resistant. In these scenarios, methicillin and vancomycin are the only available treatment options. (Link to Page on Antibiotic Structures)

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Tracking Antibiotic Resistance in Staphylococcos
Treatment of S. aureus infections showing no signs of broad-antibiotic resistance is achieved with a cocktail of antibiotics, including some of the following: flucloxacillin, gentamycin, rifamicin, fusidic acid, erythromycin, vancomyin, and cefotaxime. However, 90% of S. aureus strains are penicillin resistant. In these scenarios, methicillin and vancomycin are the only available treatment options.(See inset on antibiotic strategies for treating S. aureus-related infections)



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S. epidermis
S. epidermis is a coagulase-negative bacteria. Like S. aureus, S. epidermis is a common cause of nosocomial infections, particularly blood infections which can lead to complications of the central nervous system. S. epidermis resides primarily in the skin, leaving those who have frequent contact with needles and other invasive health care appliances particularly susceptible to illness.(2) S. epidermis is very likely to contaminate patient-care equipment and environmental surfaces, possibly explaining the high incidence of S. epidermis in hospital settings. While there is extensive information concerning S. aureus virulence factors, there is relatively little known about S. epidermis mode of action.(8) Infection is treated primarily with vancomycin or rifampin.

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S. saprophyticus
S. saprophyticus is a common cause of urinary tract infections in men and women. Risk factors and treatment guidelines are the same as those described for S. aureus.

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Tracking Antibiotic Resistance in Staphylococcus

In 1929, Alexander Flemming first discovered penicillin, but it was not until 1940 that it was fully integrated into infectious disease treatment strategies. In the intervening decade, the medical world saw the discovery of a variety of antibiotic agents. Among the most successful were the sulfonamides, prodrugs that arrested infection by inhibiting nucleic acid biosynthesis.

Sulfonamides
Sulfonamides are“prodrugs.” These compounds are made active once ingested. The sulfonamides inhibit nucleic acid synthesis by prevening the synthesis of purine bases. (6)

With the successful use of penicillin and sulfonamides, the 1940s were dubbed the antibiotic age. Suddenly, there were a wealth of ways (comparatively) to combat infectious disease. Penicillin was seen as the “cure-all.”

By 1944, however, there were dark clouds moving into an otherwise sunny picture. Strains of Staphylococcus, S. aureus particularly, were becoming resistant to penicillin. These penicillin-resistant strains produced penicillinase, a b-lactamase, that deactivated the drug by cleaving a bond in the b-lactam ring. By 1947, Staphylococcus and gonorrhea were completely resistant to penicillin. It was not until 1960 that researchers had developed new drugs that were resistant to b-lactamase activities and capable of fighting Staphylococcus infections. These new drugs, such as methicillin and oxacillin, were semi-synthetic penicillin derivatives, with functional groups placed in novel locations (1).

In 1975, the methicillin bubble burst with reports of methicillin-resistant S. aureus (MRSA). At this time, approximately 2.4% of all S. aureus strains were methicillin resistant. MRSA has been reported primarily in patients with severely compromised immune systems. Three cases reported in the late nineties existed in a man suffering from metastatic lung cancer and end-stage renal disease, a patient known already to be contaminated with vancomycin-resistant Enterococci, and an elderly patient requiring haemodialysis (10). Health care practitioners have been cited as the primary means of MRSA transmissioin (3).

In 1988, the first cases of vancomycin-resistant Enterococci were reported in the United States. In 1989, it was estimated that .3% of Enterococci infections were vancomycin-resistant; in 1993, the numbers had risen to 7.9%. In 1991, 29% of S. aureus strains were methicillin-resistant, and in 1996, there was a report of an S. aureus strain with intermediate vancomycin resistance (VISA or GISA).



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A Closer Look at Vancomycin Resistance
S. aureus strains acquired in the hospital are often resistant to many types of antibiotics. A significant portion of S. aureus strains are now methicillin-resistant, in addition to being resistant to other penicillin-derived drugs. For these methicillin-resistant strains, vancomycin is the only available, effective drug for treatment. However, in 1996, there were reports of strains of S. aureus with decreased susceptibility to vancomycin, labelled glycopeptide intermediate-resistant S. aureus, or vancomycin-intermediate S. aureus (GISA and VISA, respectively). In the early 1990s, vancomycin-resistant enterococci (VRE) emerged. Laboratory tests have shown that resistance, coded in the VanA, VanB and VanC genes, can be transferred from Enterococci to Staphylococcus and other gram positive bacteria (11). Were such transfer to occur in a non-laboratory controlled environment, there would be no FDA-approved, effective means of combating multi-drug resistant staph infections.

S. aureus can acquire resistance through extrachromosomal plasmids , through additional genetic information delivered by transposons, and through mutations in chromosomal genes. Resistance is achieved through a variety of mechanisms, including enzymatic inactivation of the drug (as with penicillinase , which cleaves the beta-lactam ring of penicillins), alteration of the drug target to prevent binding, and enhanced removal of the drug from the host tissue.

A mutation in the MecA gene of Staphylococcus will provide resistance to all beta-lactams. This gene codes for Penicillin Binding Protein --- a mutation in the gene prevents penicillin from effectively binding foreign particles. Resistance to beta-lactams is tested by exposing a bacterial culture to oxacillin. If the bacteria is resistant to oxacillin, it will be resistant to all beta-lactams, and quite possibly also resistant to erythromycin, gentamicin, tetracycline, and clindamycin (11).

Vancomycin resistance has been, to date, documented in enterococci, but not in staphylococcus. Enterococci are gram positive pathogens, listed as the second most common cause of hospital-acquired bacterial infections (3). They are part of the normal bacterial-makeup of the human gastrointestinal tract, and, like Staphylococci, cause infection when they enter the bloodstream. Enterococci can cause urinary tract infections, wound infections, septicaemia and endocarditis. They are naturally resistant to cephalosporins, aminoglycosides and clindamycin, but were, until recently, susceptible to vancomyciin. The vanA and vanB genes are responsible for encoding vancomycin resistance in the majority of Enterococci infections (11). Enterococci are transmitted via person-to-person contact (i.e. on the hands of a health care provider), or through indirect contact (i.e. through contaminated environmental surfaces) (12). The vanA and vanB genes are responsible for resistance transmittance; vanC is a chromosomal gene that cannot be transmitted between gram positive organisms (11).

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The Origins of Resistance


Infection with vancomycin-intermediate S. aureus, methicillin-resistant S. aureus, and vancomycin-resistant Enterococcus is more frequent in individuals previously treated with vancomycin or an aggressive antimicrobial therapy, individuals with severe underlying disease and immunosuppression, and indivudals recovering from intraabominal surgery (14). The spread of these pathogens is associated with overuse of antimicrobials (i.e. the prescription of broad-based antibiotics in all situations) and insufficient identification and isolation of contaminated individuals (15).

The emergence of vancomycin resistance has not only been attributed to environmental factors: studies show that prolonged treatment with vancomycin and the prolonged presence of glycopeptides can create a positive selection pressure for vancomycin-resistant strains of S. aureus. The vancomycin eliminates other bacteria, leaving the survivors (those with resistance) a wealth of nutrients on which to survive (17). In addition, increased antibacterial resistance has been correlated to the widespread use of antibiotics in agriculture. Livestock feeds are often enhanced with low doses of antibiotics which suppress the bacterial flora of the gastrointestinal tract of animals, thereby increasing the possible nutrient uptake. Antibiotics also enhance growth in livestock. Despite the benefits that such broad-spectrum use of antibiotics affords the agriculture industry, the prolonged usage of antibiotics affords bacteria the opportunity to develop resistance at a quickened pace. These resistant bacteria can be transferred to humans via contaminated food and direct contact (3).

Although the vanA and vanB genes are responsible for vancomycin-resistance in MRSA, it appears that VISA strains have a decreased susceptibility to vancomycin due to increased cell-wall material, protecting the bacteria from vancomycin’s ability to disrupt cell wall biosynthesis (17).

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Vancomycin Resistance and the Public Health Threat
“The emergence of vancomycin resistant S. aureus would represent the most important issue in antibiotic resistance since the dawn of the antibiotic era. A common, virulent, and transmissible bacterial agent with no known effective therapy would set infectious diseases back 60 years.”(4)

Prior to the age of antibiotics and the implementation of penicillin in infectious disease treatment, S. aureus infectious were a serious cause of septic shock and death following surgery. As S. aureus has acquired resistance to penicillin, and then semi-synthetic penicillin derivatives, such as methicillin, vancomycin remains the only drug to which the infection is susceptible. Were vancomycin resistance to be achieved in S. aureus, without an alternative drug therapy, it is likely that septic shock and death would once again be leading causes of mortality in individuals with compromised immune systems. In addition, the emergence of antibacterial resistant infections are likely to be costly and allow the reemergence of eradicated diseases in new, and more potent forms (such as tuberculosis) (13).

Given this threat, and the enormous financial toll that antibiotic resistant diseases already take on the American health care system, there have been a series of recommendations issued on how to deal with the emerging problem of vancomycin resistance in Staphylococcus.

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Combating Vancomycin Resistance in S. aureus
The World Health Organization and Centers for Disease Control have issued a series of extensive guidelines concerning the containment of vancomycin-resistant infections. The aim of these guidelines is to curb the development of antibacterial-resistant infections before they have evolved total resistance to all currently approved antibacterials. These guidelines are focused around three areas of improvement: 1) education of health care practitioners concerning the appropriate use of vancomycin and other broad-spectrum antibiotics; 2) implementation of systematic procedures for identification and isolation of resistant infections; 3) encourage the prudent use of vancomycin (18).

A key aspect of all guidelines concerning vancomycin-resistance containment is the isolation of individuals with resistance, or intermediate-resistant strains of the pathogen. As it is highly contagious, it is essential that infected individuals be placed in complete isolation, and that the health care practitioners interacting with these individuals be kept at a minimum (4).

A second key point is the prudent use of vancomycin. Numerous studies have reported the correlation between prolonged vancomycin use and the development of vancomycin resistance. In order to ensure prudent use of the drug, it has been suggested that all health care practitioners receive extensive training on the guidelines for proper use of the drug. These guidelines are layed out extensively at ftp://ftp.cdc.gov/pub/infectious_diseases/brochures/vancomy.txt.

The policy approach to combating vancomycin resistance is not the only means by which the medical communicty has chosen to attack this potent pathogen. New drugs, such as “WO9967256A1,” shown below, are being developed which have shown activity against methicillin-resistant S. aureus and VRE. The development of these drugs has been enhanced by new ways of modeling the sites of drug binding on the bacteria.
Structures from www.derwent.com/chemistry/articles/antibiotic.html (19)



There have also been preliminary investigations into the development of a Staphylococcus vaccine. The vaccine under study aims to attack S. aureus before it releases the toxins which cause the disease-symptoms: unlike antibiotics, which approach the toxin after it has made itself apparent, a vaccine would save people the unpleasantness of disease (20). The vaccine is built around two proteins involved in the production of S. aureus toxins: RAP (RNAIII-activating protein), and RIP (RNAIII-inhibiting protein). RAP is responsible for the activation of RNAIII, which regulates transcription of genes encoding for bacterial toxins; RIP inhibits this transcription by blocking the ability of RAP to activate RNAIII (20). Mice injected with RAP developed antibodies which then attacked RAP molecules in S. aureus, thereby preventing the production of bacterial toxins.

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References and Links
1. Duong, D., Grimes, B., and Thompson, D. Methicillin-Resistant Staphylococcus Aureus. Available online at www.rlc.dcccd.edu/mathsci/reynolds/nosocom/mrsa.html.

2. Staphylococcus. University of Texas – Houstin Medical School, DPALM MEDIC. Available online at http://medic.med.uth.tmc.edu/path/00001456.html.

3. Bogle, Bob R., and Bogle, Graciela S. Acquiring Vancomycin-Resistant Enterococcus (VRE). ADVANCE for Medical Laboratory Professionals 1997;9.

4. Edmond, M.B., Wenzel, R.P., and Pasculle, A.W. Vancomycin-Resistant Staphylococcus aureus: Perspectives on Measures Needed for Control. Available online at www.md.ucl.ac.be/didac/hosp/vanco.html.

5. Decker, J.M. MIC 421B Microbiological Techniques.http://microvet.arizona.edu/Courses/MIC421B/MIC421BgramPosCocci.html.

6. Coppoc, G.L. Introduction to Antimicrobial Drugs. Purdue Research Foundation, 1996. Available online at http://vet.purdue.edu/depts/bms/courses/chmrx/intmicr.html.

7. Aoki, K., Oguchi, A., Hosoyama, A., Nagai, Y., Kuroda, M., Hiramatsu, K., and Kikuchi, H. Staphylococcus aureus N35, complete genome. 2001. Available online at

http://www.ncbi.nlm.nih.gov/cgi-bin/Entrez/framik?db=Genome&gi=179.

8. Foster, T. Staphylococcus. Medmicro, Chapter 12. Available online at http://gsbs.utmb.edu/microbook/cho012.html.

9. Todar, Kenneth. Bacteriology 330 Lecture Topics: Staphylococcus. 1998. Available online at http://www.bact/wisc.edu/Bact330/lecturestaph.

10. Paterson, David L. Reduced susceptibility of Staphylococcus aureus to vancomycin – A review of current knowledge. Communicable Diseases Intelligence, 2001; 23. Available online at http://www.health.gov.au/pubhlth/cdi/cdi2303/cdi2303a.html.

11. Drugs and Bugs: Antibiotic Resistance Mechanisms. Available online at http://members.nbci.com/krbush/gps.html.

12. Vancomycin Resistant Enterococcus (VRE). Available online at http://www.lambtonhealth.on.ca/cdci/VRE.html

13. Lieberman, P.B., Wootan, M.G. Protecting the Crown Jewels of Medicine. Available online at http://www.cspinet.org/reports/abiotic.html.

14. Goldman, D.A., Gilchrist, M.J., Mayhall, C.G., McCormick, R.D., Edmiston, C.E., Maki, D.G., Tablan, O.C., Tenover, F.C., Martone, W.M., Gaynes, R.F., Jarvis, W.R., and Favero, M.F. Recommendations for Preventing the Spread of Vancomycin Resistance. Available online at ftp://ftp.cdc.gov/pub/infectious_diseases/brochures/vancomy.txt.

15. Lewis, Ricki. The Rise of Antibiotic-Resistant Infections. FDA Consumer Magazine. 1995; September. Available online at http://www.fda.gov/fdac/features/795_antibio.html.

16. Glycopeptide Intermediate-Resistant Staphylococcus Aureus. http://www.nfid.org/factsheets/staph.html.

17. Waldvogel, F.A. New Resistance in Staphylococcus aureus. http://www.nejm.org/content/1999/0340/0007/0556.asp.

18. See Reference 14.

19. Garton, P. Antibiotic Resistant Bacteria and Drug Strategies. Available online at http://www.derwent.com/chemistry/articles/antibiotic.html.

20. Wyman, J. Novel Strategy Found to Fight Staph Infections. http://www.niaid.nih.gov/publications/dateline/0998/PAGE2.html.