It was reported in a published article that a 49-year-old man developed a tiny papule on the tip of his nose. During the next 4 days, his nose became painful and swollen. The lesion increased in size despite treatment with trimethoprim-sulfamethoxazole. Nineteen days before his symptoms began, the patient had received the MMR (manufacturer unspecified) for deployment request. The patient had had the same female sexual partner for 2 years and had no history of oral or genital herpes simplex virus (HSV) infection. The patient's temperature was 38.4 degrees C (101.1 degrees F), but he did not have toxic appearance. He had an eschar that had no sensation on the tip of his nose and distal nasal bridge. The patient had no oral, labial, genital, or perianal ulcers. Nasal endoscopy revealed a normal nasal septum. Surface cultures of the lesion yielded scant coagulase-negative Staphylococcus and Propionibacterium acnes. Blood cultures were sterile. An assay for Human immunodeficiency virus (HIV-I) antibodies and p24 antigen was negative. An assay for serum IgG antibodies to HSV-I was negative, but an assay for serum IgG antibodies to HSV-2 was positive. Polymerase chain reaction performed on a surface swab specimen of the nose was positive for HSV-2 DNA and negative for HSV-1 and varicella-zoster virus DNA. Frozen specimens of nasal tissue obtained by surgical debridement revealed extensive necrosis and vascular thrombosis consistent with necrotizing fasciitis. Further pathology examination of these specimens revealed the effects of herpes infection. The patient received additional debridement and acyclovir, 10mg/kg of body weight every 8 hours for 10 days. After 4 weeks, the patient had almost complete reepithelialization of his nose. The author stated that this case probably represented an HSV-2 reactivation. They also stated that in this case, a temporal association existed between the MMR (manufacturer unspecified) vaccination and the patient's illness. Also that although this association may be coincidental, events that activate the immune system such as inoculation with live virus vaccines, could trigger reactivation of herpes viruses. The author said that to the best of their knowledge, nasal reactivation of HSV-2 had not been previously reported. In contrast, varicella-zoster virus could reactivate in the nasociliary branch of the trigeminal nerve and was known as herpes zoster ophthalmicus. This condition could cause vesicles to develop on the nose, which were known as Hutchinson sign; vesicles could also develop on the forehead and periocular area. Necrotizing fasciitis due to group A B-hemolytic Streptococcus occurred when as a complication of infection with varicella virus (chicken-pox) in children and as a complication of infection with varicella-zoster virus (shingles) in adults. However, the authors could not identify a causative bacterium in this case. Although HSV-2 caused necrosis of infected cells, why it causes extensive necrosis and tissue destruction only in rare cases was unclear. The article conclusion was: "Infection with HSV-2 is a lifelong condition that many persons have. This case report describes a novel manifestation with HSV-2 and should alert clinicians that herpes virus reactivation can occur in unusual anatomical locations and mimic necrotizing fasciitis". Additional information has been requested.