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INTRODUCTION: Cardiovascular implantable electronic devices (CIEDs) are being increasingly used in the primary and secondary prevention of malignant ventricular arrhythmias and conduction system disorders. Infectious complications associated with CIEDs include infective endocarditis, lead infections, and pocket-site infections, primarily involving Staphylococcus species. Infective endocarditis is a rare but life-threatening complication of gonococcal bacteremia. We report the first case of a CIED pocket-site infection secondary to Neisseria gonorrhoeae (N. gonorrhoeae). CASE: A 56-year-old male with a history of congestive heart failure status postimplantable cardioverter-defibrillator (ICD) insertion presented with a pocket-site swelling initially concerning for a hematoma which began to exhibit erythema and tenderness. The patient reported a history of high-risk sexual behavior. On presentation, he was afebrile and hemodynamically stable. Physical exam showed a 5 cm × 6 cm pocket-site swelling with overlying erythema. Labs revealed elevated ESR and CRP levels. Transthoracic and transesophageal echocardiography was concerning for infective endocarditis and lead vegetations. Blood cultures tested positive for N. gonorrhoeae. He underwent surgical debridement with complete ICD extraction and drainage of infected serosanguineous pocket fluid. Tissue cultures were negative, but isolation of N. gonorrhoeae in blood cultures confirmed it as the causative agent of the pocket-site infection in the absence of prior Gram-positive coverage. He was started on a prolonged course of ceftriaxone for 4 weeks with reimplantation of ICD at a different site after completion of treatment. CONCLUSION: In patients with high-risk sexual behavior, gonococcal bacteremia can potentially lead to CIED infection. These individuals should be prudently evaluated for infective endocarditis or pocket-site infections as presenting complaints can be subtle.
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OBJECTIVE: To report a case of famciclovir-induced leukocytoclastic vasculitis (LCV). CASE SUMMARY: A 67-year-old white female presented to the hospital for evaluation of large, bilateral palpable purpura; coalescing ulcers with central eschars; and small, red violaceous papules on her legs and groin. Approximately 2 months prior to this hospitalization, the woman was diagnosed with shingles of her left T1-T2 nerve distribution and was treated with famciclovir 500 mg 3 times daily, which was her first exposure to this medication. Her shingles resolved; however, on day 4 of treatment, she began to notice red spots on both of her legs that began to progressively blister and increase in size. She discontinued famciclovir at that time. The rash persisted and spread to her abdomen, groin, legs, feet, and toes. She underwent punch biopsy that revealed LCV. Workup was negative for antinuclear antibody, rheumatoid factor, hepatitis B and C virus, perinuclear-staining antineutrophil cytoplasmic antibodies, cytoplasmic-staining antineutrophil cytoplasmic antibodies, antibodies to extractable nuclear antigens, proteinase 3, and myeloperoxidase. The patient improved with daily oral steroids and local wound care. DISCUSSION: LCV has been reported only once before in the English literature as of January 2008. The most common cause of LCV is medication use, but it is a diagnosis of exclusion. It is hypothesized that drugs act as haptens, which cause an immune response. An objective causality assessment using the Naranjo probability scale suggested that famciclovir was the probable cause of LCV in this patient. CONCLUSIONS: Healthcare professionals should be aware of the possible development of famciclovir-induced LCV.