Re: staph infection

What is a staph infection?
It is a type of infection caused by a Staphylococcus (or "staph") bacteria. Actually, about 25% of people normally carry staph in the nose, mouth, genitals, and anal area. The foot is also very prone to pick up bacteria from the floor. The infection often begins with a little cut, which gets infected with bacteria.

These staph infections range from a simple boil to antibiotic-resistant infections to flesh-eating infections. The difference between all these is how deep and how fast the infection spreads, and how treatable it is with Antibiotics . The antibiotic-resistant infections are more common in North America, because of our overuse of Antibiotics .

The type of staph infection that involves skin is called cellulitis and affects the skin's deeper layers. It is treatable with Antibiotics .

This type of infection is very common in the general population -- and more common and more severe in people with weak immune systems. People who have diabetes or weakened immunity are particularly prone to developing cellulitis.

What Are the Symptoms of Staph Infection?
Staph cellulitis usually begins as a small area of tenderness, swelling, and redness. Sometimes it begins with an open sore. Other times, there is no break in the skin at all -- and it's anyone's guess where the bacteria came from.

The signs of cellulitis are those of any inflammation -- redness, warmth, swelling, and pain. Any skin sore or ulcer that has these signs may be developing cellulitis. If the staph infection spreads, the person may develop a fever, sometimes with chills and sweats, as well as swelling in the area.

What’s the Treatment for Staph Infection?
Antibiotics are used to treat these infections. But there's been a gradual change in how well these antibiotics work. While most staph infections used to be treatable with penicillin, in the 1980s that changed and stronger antibiotics are now used.

In about 50% of cases, however, resistance is seen to even these stronger antibiotics. These cases are not just happening in hospitals -- as once was true -- but now are occurring in the general community. That's been a problem. Many doctors are accustomed to using certain antibiotics, but those then fail because of Antibiotic resistance. There are several more potent antibiotics now, but doctors need to know when to use them.

There's another treatment sometimes used with staph infections. If the infection goes so deep that it involves muscles or fibers that enclose muscles, it needs to be surgically cleaned.

Can Staph Infection Be Prevented?
You can take steps to help prevent it. Any time you have a cut or skin breakdown, wash it with soap and water, keep it clean and dry, use antiseptic ointment, and keep it covered. A couple of recent outbreaks among football players began when one team member had a boil, and the infection was spread to other team members.

The staph infection is contagious if the wound is weeping or draining, and if people share towels or other items that are contaminated. Wearing foot coverings in locker rooms and other commonly used areas can help prevent contamination.

If the sore becomes unusually painful or red, get prompt medical attention. If red lines develop, that's a sign the infection is spreading and needs immediate medical attention.

Exfoliative Toxins and the Skin

Recently, ETs were shown to stimulate the skin associated lymphoid tissue (SALT) by demonstrating that the toxins activated murine splenic T cells in the presence of Langerhans' cells and MHC class II-bearing keratinocytes to produce a range of cytokines, including IL-1 and tumor necrosis factor alpha, capable of stimulating other accessory and immune system cells (268). Furthermore, binding of ETs to Langerhans' cells resulted in dose-dependent depletion of these cells (as measured by the number of ATPase-positive cells per square millimeter) in cultured mouse skin, presumably due to migration of the cells to draining lymph nodes, where they may act as APCs for T lymphocytes (202). SALT is part of the immune system that deals with antigenic challenges common to the skin and includes antigen-presenting Langerhans' cells, keratinocytes, and T-cell subsets with skin-homing receptors (258). Despite the presence of MHC class II molecules, which are induced on the cell surface during inflammatory processes (273), keratinocytes are unable to act as conventional APC and seem to function only in the presence of superantigens (268). Activation of SALT by ETs may therefore result in the erythematous rash associated with SSSS. For example, there is some evidence that the ability of the superantigen TSST-1 to activate cutaneous lymphocyte-associated antigens may be responsible for the rash and desquamation seen in TSS (149), just as the superantigens of group A streptococci might play a role in the development of the characteristic cutaneous swelling, erythema, and desquamation seen in streptococcal infections (254). However, the lack of immune cells on histological specimens from patients with SSSS cannot be easily explained and requires more research. It may be that the very specific (possibly intracellular) site of action of the toxins does not allow them to exert superantigenic activity in terms of duration or location or that activation of the toxins to proteases, which probably requires a structural change (25, 44, 270), results in loss of superantigenic activity at the site of action.

The ability of the ETs to activate the SALT subpopulation of the immune system has important consequences for several dermatological conditions, including cutaneous T-cell lymphoma and atopic dermatitis. ETA is capable of inducing the proliferation of V2.1-bearing cutaneous T-cell lymphoma cells in vitro, and this proliferative response is enhanced by adding IL-1. This fits in with observations showing that activation of SALT by ETA results in IL-1 release (268), and IL-1, along with IL-6, plays an important role in enhancing the activity of other superantigens (136).

Patients with atopic dermatitis have a higher staphylococcal colonization rate than does the general population (8, 152). Antibiotic treatment of patients with atopic dermatitis has resulted in significant clinical improvement of the condition (150), suggesting that staphylococci play a role in the pathogenesis of the disease. Recently, it has been shown that a large proportion of S. aureus strains isolated from patients with atopic dermatitis release superantigens, including enterotoxins, TSST-1, and ETs (147, 167). It has been speculated that superantigens bind to surface MHC class II molecules found on keratinocytes during inflammation and thereby activate polyclonal T cells locally (257).

Exfoliative Toxins and Other Human Diseases

The V-expansion of T cells characteristic of superantigens has also been demonstrated in other conditions, where the role of staphylococcal toxins is still unclear. Kawasaki disease, also known as mucocutaneous lymph node syndrome, is a multisystem disorder in children that is characterized by fever, rash, conjunctivitis, mucosal inflammation, erythematous peeling of the hands and feet, and, rarely, coronary artery aneurysms (147, 175). A selective expansion of V2- and V8-expressing T cells has been detected in the blood of patients with Kawasaki disease (1), and, while TSST-1 has been detected in a proportion of these patients (146, 147, 148), the potential role of the ETs has not been studied. Other conditions where expansion of V-expressing T cells, often by staphylococcal superantigens, has been demonstrated include hematogenously acquired staphylococcal nephritis (138, 271), staphylococcal septic Arthritis (38, 290), various autoimmune diseases (137, 184), Rheumatoid Arthritis (197), multiple sclerosis (39, 256), contact sensitivity (228), and guttate and chronic plaque Psoriasis (151, 288); another possible role for the expansion of V-expressing T cells is in the gradual decline in the number of CD4+ T cells in human immunodeficiency virus infection (143). Unfortunately, many of the studies on the superantigenic effects of ETs in various diseases have used commercially prepared toxins, which, as many authors have pointed out, may be contaminated by other superantigens. Future studies should take this factor into consideration and use appropriate precautions to eliminate the problem.

Several other conditions have demonstrated a significant association with staphylococcal toxins; sudden infant death syndrome (SIDS) is probably one of the most important (31). S. aureus strains producing multiple toxins have been isolated from infants with SIDS (265). In addition, S. aureus is the most common organism isolated from 2- to 4-month-old infants, being found in almost 50% of the infants (222). This age group is also associated with the highest incidence of SIDS (31). Lee et al. (145) have shown that bacterial isolates, particularly S. aureus and Escherichia coli, from infants with SIDS were lethal to gnotobiotic rats. Therefore, some authors have proposed that common bacterial toxins absorbed through the respiratory tract might be involved (182). Furthermore, staphylococcal infection in combination with influenza virus infection was shown to greatly increase the production of SE, resulting in an exaggerated inflammatory response in ferrets (117). This activity might explain the higher prevalence of SIDS in winter (43). Although TSST-1 was demonstrated in renal tubular cells of some infants with SIDS but not control infants (189), the role of the ETs in SIDS has, unfortunately, never been studied. It is possible that an abnormal inflammatory response due to the superantigenic properties of the ETs, which may be produced locally in the nasopharynx and then systemically absorbed (189), coupled with enhancement by concurrent viral infection will result in sudden death in infants.