What is mercer Staph? What causes it? Is it cureable? Contagious?

Answer 1

MRSA commonly called Mersa.
But most of these antibiotics don’t work against a highly resistant type of staph called MRSA (Mersa)--Methicillin Resistant Staph Aureus. This highly antibiotic resistant bug has been around for 40 years, and has affected for the most part very sick individuals who are hospitalized, such as those with iv lines that pierce the skin, or urinary catheters.
Usually it affects intensive care unit patients
They are so serious, that almost a quarter of the infections, of which most are skin infections, require hospitalization. Fortunately, there are some antibiotics which will work, including this one, vancomycin, which must be given intravenously.

Answer 2

Mercer Staph

Answer 3

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Answer 4

MRSA Means Methicillin resistant staph Aureus. It means the staph is resistant to the antibiotic methicillin. And it is contagious, and you have to give a different antibiotic to cure the staph....

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Answer 6

Staph (pronounced "staff") is medical quick speak for staphylococcus aureus bacteria. This pesky little bacterium is very common (many people have some living on their skin all the time), but when it enters the human body, usually through an open cut or break in the skin, it can cause infection and trouble anywhere in the body. Staph infections tend to be pus-producing. Common minor (or relatively minor) skin infections caused by staph include:

Folliculitis
Infections of hair follicles that cause itchy white pus-filled bumps on the skin (often where people shave or have irritations from skin rubbing against clothes)

Boils
Infections deeper within hair follicles that leave large, frequently red inflammations (often occur on the face or neck)

Sties
Infection of the follicle surrounding the eyelashes, causing a sore red bump in the eyelid

Impetigo
The infection kids often get around their mouths and noses that causes blisters and red scabby skin

Abscesses
Infection characterized by pus and swelling that can occur in the skin and in any other organ.

Staph infection is also the leading culprit behind cases of food poisoning, and can be to blame for larger life threatening conditions, such as Toxic Shock Syndrome (TSS), pneumonia, bone infections (osteomyelitis), mastitis in nursing mothers, endocarditis (infection of the inside of the heart), and bacteremia (blood infection). People who are otherwise healthy typically do not usually become severely ill from staph infections, but those at special risk, who have weakened immune systems, include:

persons with chronic illnesses, such as diabetes, cancer, lung disease, kidney disease, or HIV/AIDS
people with various skin conditions
the elderly
newborns
people recovering from major surgery
injection drug users (especially those who reuse needles)
people whose immune systems are weakened due to steroid use, radiation therapy, cancer treatment, immunosuppressive medications
women who are breastfeeding
Health care professionals can determine that staph (and not some other bacteria) is the cause of an infection by taking a culture (usually a swab from what looks like a giant Q-tip) from the infected site. Once staph has been diagnosed, the provider will prescribe antibiotics that are known to work on that specific strain of the bacteria. These antibiotics (usually either pills or creams applied to the infected body part) typically kill the bacteria and cure the infection within a week or two.

Hospitals are working to stamp out staph infections, in part because the majority of hospital patients fall into at least one "at-risk" category, but also because drug-resistant strains of staph (versions of the bacteria that aren't killed by one or more of the antibiotics that are commonly used to treat staph infections) are becoming an increasingly common threat. These drug-resistant strains of staph do not cause worse or different infections than non-resistant strains, but they can be much harder to treat because the most common (and easiest to use) antibiotics may not be effective. People with resistant staph infections may require hospitalization to receive antibiotics through an IV or by injection.

Because improper use of antibiotics can help produce resistance to drugs, making future infections much harder to treat, the American Medical Association recommends that patients:

follow the directions for any prescription exactly
take all of the medicine prescribed (even if one feels better after only a few days)
never save old, leftover prescriptions for future use
never take anyone else's prescription antibiotics
Other preventative measures are careful treatment of all skin conditions, including wound care after trauma or surgery, IV drug users taking precautions when injecting, and people with special risk factors being attentive to early symptoms of staph.

For an entire dose of the whys and wherefores of proper antibiotic use, check out the American Medical Association's fact sheet, Antibiotics: Facts You Should Know.

Answer 7

I had staph last year. My doctor cut my foot to get it out. I took shots for it everyday ffor a week. Is it possible for me toget it again cuz the other side of my foot is an has been swelling up for awhile.

Answer 8

what does sever skin conditions look like caused by mercer?

Answer 9

Try webmd website

Answer 10

Scientific classification
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Bacillales
Family: Staphylococcaceae
Genus: Staphylococcus
Species: S. aureus
Binomial name
Staphylococcus aureus
Rosenbach 1884

Staphylococcus aureus (which is occasionally given the nickname golden staph) is a bacterium, frequently living on the skin or in the nose of a healthy person, that can cause illnesses ranging from minor skin infections (such as pimples, boils, and cellulitis) and abscesses, to life-threatening diseases such as pneumonia, meningitis, endocarditis, Toxic shock syndrome (TSS), and septicemia. Each year some 500,000 patients in American hospitals contract a staphylococcal infection. It is a spherical bacterium. It is abbreviated to S. aureus or sometimes referred to as Staph aureus in medical literature, and should not be confused with the somewhat similar named streptococci which are also medically important.
Microbiology
S. aureus is a Gram-positive coccus, which appears as grape-like clusters when viewed through a microscope and as large, round, golden-yellow colonies, often with β-hemolysis, when grown on blood agar plates. The golden appearance is the eytmological root of the bacteria's name: aureus means "gold" in Latin.
S. aureus is catalase positive and thus able to convert hydrogen peroxide (H2O2) to water and oxygen, which makes the catalase test useful to distinguish staphylococci from enterococci and streptococci. S. aureus can be differentiated from most other staphylococci by the coagulase test: S. aureus is coagulase-positive, while most other Staphylococcus species are coagulase-negative.
The species has been subdivided into two subspecies: S. aureus aureus and S. aureus anaerobius. The latter requires anaerobic conditions for growth, is an infrequent cause of infection, and is rarely encountered in the clinical laboratory.
Treatment and the development of antibiotic resistance
Antibiotic resistance in S. aureus was almost unknown when penicillin was first introduced in 1943; indeed, the original petri dish on which Alexander Fleming observed the antibacterial activity of the penicillium mould was growing a culture of S. aureus. By 1950, 40% of hospital S. aureus isolates were penicillin reisistant; and by 1960, this had risen to 80%.[1]
Today, S. aureus has become resistant to many commonly used antibiotics. In the UK, only 2% of all S. aureus isolates are sensitive to penicillin with a similar picture in the rest of the world. The β-lactamase resistant penicillins (methicillin, oxacillin, cloxacillin and flucloxacillin) were developed to treat penicillin-resistant S. aureus and are still used as first-line treatment. Methicillin was the first antibiotic in this class to be used (it was introduced in 1959), but only two years later, the first case of methicillin-resistant S. aureus (MRSA) was reported in England.[2] Despite this, MRSA generally remained an uncommon finding even in hospital settings until the 1990's when there was an explosion in MRSA prevalence in hospitals where it is now endemic.[
First line treatment for MRSA is currently glycopeptide antibiotics (vancomycin and teicoplanin). There are number of problems with these antibiotics, mainly centred around the need for intravenous administration (there is no oral preparation available), toxicity and the need to monitor drug levels regularly by means of blood tests. There are also concerns that glycopeptide antibiotics do not penetrate very well into infected tissues (this is a particular concern with infections of the brain and meninges and in endocarditis). Glycopeptides must not be used to treat methicillin-sensitive S. aureus as outcomes are inferior.
In situations where the incidence of MRSA infections is known to be high, the attending physician may choose to use a glycopeptide antibiotic until the identity of the infecting organism is known. When the infection is confirmed to be due to a methicillin-susceptible strain of S. aureus, then treatment can be changed to flucloxacillin or even penicillin as appropriate.
Vancomycin-resistant S. aureus (VRSA) is a strain of S. aureus that has become resistant to the glycopeptides. The first case of vancomycin-intermediate S. aureus (VISA) was reported in Japan in 1996;[5] but the first case of S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.[6] Three cases of VRSA infection have been reported in the United States.
Mechanisms of antibiotic resistance
For more details on this topic, see Methicillin-resistant Staphylococcus aureus.
Staphylococcal resistance to penicillin and cephalosporins is mediated by β-lactamase production: enzymes which break down the β-lactam ring of the penicillin molecule. β-lactamase-resistant penicillins such as methicillin, oxacillin, cloxacillin and flucloxacillin are able to resist degradation by staphylococcal β-lacatamase.
The mechanism of resistance to methicillin is by the acquisition of the mecA gene, which codes for an altered penicillin-binding protein (ABP) that fails to bind β-lactams (penicillins, cephalosporins and carbapenems).
Glycopeptide resistance is mediated by acquisition of the vanA gene. The vanA gene originates from the enterococci and codes for an enzyme that produces an alternative peptidoglycan that vancomycin will not bind to.
Role in disease
S. aureus may occur as a commensal on human skin (particularly the scalp, armpits and groins); it also occurs in the nose and throat and less commonly, may be found in the colon and in urine. The finding of Staph. aureus under these circumstances does not always indicate infection and therefore does not always require treatment (indeed, treatment may be ineffective and re-colonisation may occur). It can survive on domesticated animals such as dogs, cats and horses, but has never been found on food animals such as poultry or swine. It can survive for some hours on dry environmental surfaces, but the importance of the environment in spread of Staph. aureus is currently debated.
S. aureus can infect other tissues when normal barriers have been breached (e.g. skin or mucosal lining). This leads to furuncles (boils) and carbuncles (a collection of furuncles). In infants S. aureus infection can cause a severe disease Staphylococcal scalded skin syndrome (SSSS).[8]
S. aureus infections can be spread through contact with pus from an infected wound, skin-to-skin contact with an infected person, and contact with objects such as towels, sheets, clothing, or athletic equipment used by an infected person.
Deeply situated S. aureus infections can be very severe. Prosthetic joints put a person at particular risk for septic arthritis, and staphylococcal endocarditis (infection of the heart valves) and pneumonia may be rapidly fatal.
Staphylococcus aureus and influenza
S. aureus superinfection is an uncommon complication of influenza. However, in the last three influenza pandemics (1918, 1957–58, and 1968), added infection with S. aureus was an important cause of increased morbidity and mortality from this disease.
Toxic Shock Syndrome
S. aureus is also the causative agent for Toxic Shock Syndrome.
Infection control
Spread of S. aureus (including MRSA) is through human-to-human contact, with environmental contamination thought to play a relatively unimportant part. Emphasis on basic hand washing techniques are therefore effective in preventing the transmission of S. aureus. The use of disposable aprons and gloves by staff reduces skin-to-skin contact and therefore further reduces the risk of transmission. Please refer to the chapter on infection control for further details.
Staff or patients who are found to carry resistant strains of S. aureus may be required to undergo "eradication therapy" usually which may include antiseptic washes and shampoos (such as chlorhexidine) and application of topical antibiotic ointments (such as mupirocin or neomycin) to the anterior nares of the nose.
Role of pigment in virulence
The vivid yellow pigmentation of S. aureus may be a factor in its virulence. When comparing a normal strain of Staph. aureus with a strain modified to lack the yellow coloration, the pigmented strain was more likely to survive dousing with an oxidizing chemical such as hydrogen peroxide than the mutant strain was.
Colonies of the two strains were also exposed to human neutrophils. The mutant colonies quickly succumbed while many of the pigmented colonies survived. Wounds on mice were swiped with the two strains. The pigmented strains created lingering abscesses. Wounds with the unpigmented strains healed quickly.
These tests suggest that the yellow pigment may be key to the ability of S. aureus to survive immune system attacks. Drugs that inhibit the bacterium's production of the carotenoids responsible for the yellow coloration may weaken it and renew its susceptibility to antibiotics.