Ecthyma Gangrenosum

Ecthyma gangrenosum develops after bacteria invade small blood vessels in the skin and underlying subcutaneous tissue. Bacterial invasion usually happens due to the proliferation of a systemic infection through the bloodstream, but it can also occur by direct entry of bacteria through a skin wound. The infection damages the blood vessel walls, which reduces blood supply to the skin and subcutaneous tissue. This results in redness, edema, and necrosis (i.e., tissue death) of the skin, with subsequent ulcer formation. 

Traditionally, ecthyma gangrenosum has been associated with the bacteria Pseudomonas aeruginosa; however, more recently, ecthyma gangrenosum-like lesions have been reported on individuals who have other bacterial, fungal, or viral infections. Causative microorganisms include gram-positive bacteria, like Staphylococcus aureus, Streptococcus pyogenes, and Klebsiella pneumoniae; fungi, such as Mucor and Candida species; and the herpes simplex virus (HSV). 

Initial medical treatment, sometimes begun prior to confirmation of the infectious agent, generally involves a combination of antibiotics that target Pseudomonas aeruginosa, including antipseudomonal penicillins (e.g., piperacillin/tazobactam), aminoglycosides (e.g., gentamicin), quinolones (e.g., levofloxacin), third-generation cephalosporins (e.g., ceftazidime, cefepime), or carbapenems (e.g., imipenem, meropenem). Once the infectious agent and antibiotic susceptibilities are identified, the antibiotic therapy may need to be adjusted. In the rare cases of fungal or viral infections, treatment may include systemic antifungal therapy (e.g., azoles, amphotericin B) or specific antiviral agents. 

In cases where ecthyma gangrenosum fails to respond to medication, surgical removal of any dead, damaged, or infected tissue may be necessary to completely resolve the infection.