Staphlyococcus aureus, or "staph", is possibly the world's most common bacteria. The name Staphlyococcus refers to the clusters that the bacteria form when they multiply, which can be seen easily under a microscope. Aureus is Latin for "golden"; clusters of S. aureus grown in culture in the laboratory are golden-yellow.
S. aureus is found just about everywhere -- including walls, floors, furniture, and other surfaces, and including many areas of human and animal bodies. For example, we all have S. aureus on our skin, and in other places on our bodies, such as in our nostrils. Normally this isn't a big problem: if our skin is intact bacteria can't penetrate to cause an active infection, and even in the nose and mouth bacteria can just sit around without causing a full-blown infection.
However, S. aureus and other bacteria can enter the skin and the body through small breaks (like abrasions, lacerations, and puncture wounds, and even the cracks that often happen in very dry skin). If S. aureus enters and starts multiplying, pus (an accumulation of white blood cells) may form at the infected site. A small accumulation of pus in a bump on the skin is called a pustule. A larger accumulation may become an abscess, which is a mass of pus, with or without bacteria, surrounded by a wall that the body forms to try and isolate the infection. An abscess can form anywhere in the body, including fatty tissues, muscles, organs such as the liver or the lungs, and even in the brain.
Although the abscess may limit spread of the infection, the abscess wall can keep white blood cells and other components of the immune system from getting to the bacteria. Therefore, larger abscesses may need to be opened (with a scalpel or a large needle) and the fluid inside drained. This may be necessary whether or not a patient is given antibiotics for the infection -- in fact, antibiotics may not be able to penetrate into an abscess either.
S. aureus is notoriously good at becoming resistant to antibiotics, either by mutating or, in some cases, by picking up genes from other bacteria that make the other bacteria resistant. It is very rare nowadays to find a specimen of S. aureus that is not resistant to the simpler penicillins. Modified penicillins, of which the first was methicillin, were developed beginning in the late 1950's to treat penicillin-resistant S. aureus infections. Within one year after methicillin went on the market, strains of S. aureus that were resistant to methicillin and its relatives, and to the cephalosporins (which are chemically similar to the penicillins) became common. These strains are known as methicillin-resistant S. aureus, or MRSA. MRSA has become more and more prevalent over the years: a study published in the January, 2009 issue of Archives of Otolaryngology - Head & Neck Surgery (volume 135, issue 1, pages 14-16)) reports that over 28% of staphylococcal infections of the head and neck (the middle ear, ear canal, nose, mouth, throat, sinuses, and neck) seen in 2006 were caused by MRSA -- an increase of over 16% over six years.
Five different families of MRSA have been identified, all of which are resistant to penicillins and cephalosporins. However, MRSA from some of these families can be treated with certain other antibiotics. In particular, one family of MRSA, the USA-300 genotype (a genotype is a genetic family), is susceptible to trimethoprim and sulfamethoxazole (TMP-SMX), and we commonly treat suspected MRSA infections with TMP-SMX to start with, changing only if the infection doesn't respond. Most S. aureus found in the United States, even MRSA, are still susceptible to other antibiotics such as vancomycin, one of the antibiotics of last resort (partly because of its side effects). In some countries, though, doctors have seen patients with vancomycin-resistant S. aureus, or VRSA -- which could easily kill a severely-infected patient simply because there isn't much else we can use to treat the infection.
One easy way to make bacteria resistant to an antibiotic is to stop taking the antibiotic too early. This lets the "stronger" bacteria -- those that have developed a little tolerance to the antibiotic through mutation or gene-trading with other bacteria -- multiply and continue to develop their resistance mechanisms. This is why, when you are given antibiotics for an infection, you MUST finish all of the antibiotics you are given, even if you feel better. Resistant bacteria often become resistant either because they were given to patients who did not need the antibiotic in the first place, or because they were not given or taken in the right dose or for the right length of time.
Preventing a MRSA infection doesn't usually require antibiotics. Most of the time, all it takes is soap and water. Keeping your hands clean can help prevent spreading MRSA, and other infections as well, from an infected person to someone else. If you don't have soap and water around, the alcohol-based hand cleaner gels do a pretty good job of killing bacteria on the skin. This is especially important for us doctors, and anyone else who works with -- or just visits -- sick patients. Hospitals require us to wash our hands before and after seeing and examing a patient precisely to reduce the chances of taking MRSA or another resistant bacteria from one patient to another. (It's also important to moisturize your hands regularly so that all that handwashing doesn't cause breaks in your skin and lead to a MRSA infection.) You should also be careful about pustules or boils on the skin of other people -- and on animals, even your pet cats. (The US Centers for Disease Control and Prevention have reported cases of MRSA transmission involving pets, including this case of transmission of MRSA between a cat and his owner.)