Diagnosis
Erysipelas is usually diagnosed by the clinician looking at the characteristic well-demarcated rash following a history of injury or recognition of one of the risk factors.Tests, if performed, may show a high white cell count, raised CRP or positive blood culture identifying the organism.Erysipelas must be differentiated from herpes zoster, angioedema, contact dermatitis, erythema chronicum migrans of early Lyme disease, gout, septic arthritis, septic bursitis, vasculitis, allergic reaction to an insect bite, acute drug reaction, deep venous thrombosis and diffuse inflammatory carcinoma of the breast. Differentiating from cellulitis
Erysipelas can be distinguished from cellulitis by two particular features; its raised advancing edge and its sharp borders. The redness in cellulitis is not raised and its border is relatively indistinct. Bright redness of erysipelas has been described as a third differentiating feature.Erysipelas does not affect subcutaneous tissue. It does not release pus, only serum or serous fluid. Subcutaneous edema may lead the physician to misdiagnose it as cellulitis. Treatment
Depending on the severity, treatment involves either oral or intravenous antibiotics, using penicillins, clindamycin, or erythromycin. While illness symptoms resolve in a day or two, the skin may take weeks to return to normal. The USA Food and Drug Administration has approved 4 antibiotics-- omadacycline (Nuzyra), oritavancin (Orbactiv), dalbavancin (Dalvance), and tedizolid (Sivextro) --for the treatment of acute bacterial skin and skin structure infections. Because of the risk of reinfection, prophylactic antibiotics are sometimes used after resolution of the initial condition.
Congenital stromal corneal dystrophy (CSCD) is an extremely rare, autosomal dominant form of corneal dystrophy. Only 4 families have been reported to have the disease by 2009. The main features of the disease are numerous opaque flaky or feathery areas of clouding in the stroma that multiply with age and eventually preclude visibility of the endothelium. Strabismus or primary open angle glaucoma was noted in some of the patients. Thickness of the cornea stays the same, Descemets membrane and endothelium are relatively unaffected, but the fibrils of collagen that constitute stromal lamellae are reduced in diameter and lamellae themselves are packed significantly more tightly. Genetics
CSCD is associated with a mutation in the gene DCN that encodes the protein decorin, located at chromosome 12q22. The disorder is inherited in an autosomal dominant manner, which indicates that the defective gene responsible for a disorder is located on an autosome (chromosome 12 is an autosome), and only one copy of the gene is sufficient to cause the disorder, when inherited from a parent who has the disorder. Diagnosis
Treatment
References
External links
GeneReviews/NCBI/NIH/UW entry on Congenital Stromal Corneal Dystrophy