Necrotizing fasciitis associated with systemic lupus erythematosus in a child.

Sir,

I have two comments on the interesting case report by Srinivas et al. on the necrotizing fasciitis (NF) associated with systemic lupus erythematosus (SLE) in an Indian child.[1]

First, the authors nicely addressed the clinical presentation of the patient. The patient was diagnosed with NF based on the positive culture of the tissue and pus revealing Group A Streptococcus, Klebsiella, and Escherichia coli. The patient, unfortunately, ran a rapid deteriorating course and eventually succumbed due to sepsis despite surgical skin debridement and broad-spectrum antibiotic coverage. I presume that the rapid escalation in the clinical picture of the patient necessitates consideration of another concomitant diagnosis. It is obvious that SLE patients are more susceptible to various infections due to impaired immune response. Mucormycosis is well-known to be an invasive fungal infection caused by fungi of the order Mucorales, mainly affecting immunocompromised patients. Cutaneous mucormycosis (CM) is the third most common clinical form of the disease, after pulmonary and rhinocerebral. The agents of mucormycosis are ubiquitous in nature and are transmitted to the skin by direct inoculation, as a result of various types of trauma. These include needle sticks, stings and bites by animals, motor vehicle accidents, natural disasters, and burn injuries. The typical presentation of CM is the necrotic eschar, but it can present with various other signs. The infection can be locally invasive and penetrate into the adjacent fat, muscle, fascia, and bone, or become disseminated.[2] Up to 24% of primary CM can be complicated with NF.[3] In India, the available data pointed out that cases of CM were increasingly reported with an overall mortality of 35%. The most common zygomycete identified was Apophysomyces elegans, and the most common predisposing factor was breach of the skin.[4] It is suggested that a high index of suspicion is needed to diagnose CM. Therefore, it should always be considered among the differentials of necrotic wounds that do not respond to the conventional therapy even in immunocompetent individuals and histopathological study of tissue biopsy and culture in suitable media for fungi should be performed in suspected cases.[3] I presume that if the diagnosis of CM was considered by the authors in the case in question together with the implementation of wound debridement, antibacterial, and antifungal coverage, the rapid clinical deterioration with resultant mortality might be curtailed in the studied patient.

Second, the association between SLE and NF could be addressed in three presentations. (1) The development of NF in SLE patients could occur as a consequence of poor immunity secondary to the disease itself and the immunosuppressive therapy. (2) Patients with NF could be incidentally diagnosed to have occult SLE like the case in question. (3) It is obvious that SLE is a potentially fatal autoimmune disease involving virtually all the key components of the immune system. It is, therefore, suggested that caution should be exercised in the follow-up of NF patients because NF might immediately favor the development of a severe autoimmunity resulting in SLE.[5]

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