In addition, the presence of low mitotic activity, vascular proliferation and necrosis, including pseudopallisading necrosis, is insufficient by itself to elevate the grade of this tumor. This leads to inevitable interobserver variability in diagnosis by pathologists. The ultimate responsibility for making treatment decisions and interpretation of this diagnosis lies with the oncologist in consultation with the patient and their family. It has been proposed that WHO guidelines should contain a category for grade IV oligodendrogliomas which essentially appear to be glial neoplasms with overwhelming features of glioblastoma multiforme (GBM) arising from known lower grade oligodendrogliomas or GBM with a significant proportion of oligodendroglial differentiation. The diagnostic utility of this latter category is uncertain as these tumors may behave either like glioblastoma or grade III Anaplastic oligodendrogliomas. As such,this is an exceptionally unusual diagnosis. The updated WHO guidelines published in 2007 recommends classifying such tumors for the time being as glioblastoma with oligodendroglioma component. It remains to be established whether or not these tumors carry a better prognosis than standard glioblastomas. Molecular genetics
By far, the most common structural deformity found is co-deletion of chromosomal arms 1p and 19q. The high frequency of co-deletion is a striking feature of this glial tumour and is considered as a "genetic signature" of oligodendroglioma. Allelic losses on 1p and 19q, either separately or combined, are more common in classic oligodendrogliomas than in either astrocytomas or oligoastrocytomas.
Staphylococcal scalded skin syndrome (SSSS) is a dermatological condition caused by Staphylococcus aureus. Signs and symptoms
The disease presents with the widespread formation of fluid-filled blisters that are thin walled and easily ruptured, and the patient can be positive for Nikolskys sign. Ritters disease of the newborn is the most severe form of SSSS, with similar signs and symptoms. SSSS often includes a widespread painful erythroderma, often involving the face, diaper, and other intertriginous areas. Extensive areas of desquamation might be present. Perioral crusting and fissuring are seen early in the course. Unlike toxic epidermal necrolysis, SSSS spares the mucous membranes. It is most common in children under 6 years, but can be seen in adults who are immunosuppressed or have kidney failure. Pathophysiology
The syndrome is induced by epidermolytic exotoxins (exfoliatin) A and B, which are released by S. aureus and cause detachment within the epidermal layer, by breaking down the desmosomes. One of the exotoxins is encoded on the bacterial chromosome, while the other is encoded on a plasmid. These exotoxins are proteases that cleave desmoglein-1, which normally holds the granulosum and spinosum layers together, similar to the pathophysiology of the autoimmune skin disease, pemphigus vulgaris. Diagnosis
SSSS is a clinical diagnosis. This is sometimes confirmed by isolation of S. aureus from blood, mucous membranes, or skin biopsy; however, these are often negative. Skin biopsy may show separation of the superficial layer of the epidermis (intraepidermal separation), differentiating SSSS from TEN, wherein the separation occurs at the dermo-epidermal junction (subepidermal separation).