In another study, MGUS patients with none, 1, or 2 of the following risk factors, >95% of bone marrow plasma cells that are clonal in nature and a 10% or greater rise in the levels of their monoclonal proteins within 3 years, had 2, 16, and 72% risks, respectively, of progression within 7 years. However, estimates on the risks of progression for some of these parameters are tentative and subject to change. For example, the IgA form of MGUS, while once considered to have a poorer prognosis than IgG MGUS, was found to have a prognosis similar to IgG MGUS in a more recent study. IgM MGUS
While traditionally classified as such, it is not clear that IgM MGUS is a clonal plasma cell dyscrasia. IgM MGUS involves an increase in a B cell derivative with morphological features of both plasma cells and lymphocytes viz., lymphoplasmacytic  cells. Studies indicate that both plasma cells and lymphoblastic cells infiltrate involved tissues and that one or perhaps both cell types harbor mutations in a) the MYD88 gene (~20% in IgM MGUS and >90% in IgM-related malignancies), almost all of which are L265P mutations (i.e.
Cause
Exposure is most commonly seen in hospital wards and nurseries, and can be passed from person to person in other settings, such as close contact sports. Therefore, the patient is advised to try to limit human contact as much as possible to minimize the risk of spreading the infection. Infectious period
After 48 hours the disease is considered no longer contagious assuming the proper antibiotic treatments have been administered. Pathogenesis
Exfoliating toxins are serine proteases that specifically bind to and cleave desmoglein 1 (Dsg1). Previous studies suggested that exfoliating toxins bind to gangliosides, causing a release of protease by keratinocytes acting as superantigens in stimulating the skins immune system. A more recent proposal states there are three known exfoliating toxins; ETA, ETB, and ETD which act as a glutamic acid-specific serine protease with concentrated specificity. Which results in the cleavage of human Dsg1 at a unique site after glutamic acid residues causing deactivation. Proteolysis of the peptide bond leading up to the dysfunction of Dsg1 and the desmosome allows for an understanding as to why the bullous forms, making the peptide bond crucial for proper function if Dsg1. S. aureus
A phyogenic non-motile Gram-positive cocci which forms into grape like clusters. Just like other forms of staph, S. aureus has a variety of virulence factors which include surface proteins involved in adherence, secretion of enzymes that degrade proteins, and secrete toxins which damage the hosts cells.S. aureus expresses surface receptors for fibrinogen, fibronectin, and vitronectin.