B71-16 Unmasking an Immune Masquerade: Chlamydia Pneumoniae as an Unusual Trigger of Cutaneous Vasculitis

Abstract Introduction Leukocytoclastic vasculitis (LCV) is a small-vessel vasculitis primarily involving postcapillary venules, most commonly presenting as palpable purpura. It is typically triggered by infections, medications, or autoimmune disorders, with immune complex deposition leading to vessel wall inflammation. Chlamydia pneumoniae is a rare but recognized infectious cause. While primarily a respiratory pathogen, several reports have described its association with cutaneous vasculitis, including LCV. Case Presentation A 36-year-old female with a history of treated hepatitis C infection and opioid use disorder presented with a two-week history of upper respiratory symptoms followed by a painful, pruritic rash that began on the lower limbs and spread to the abdomen and upper limbs. Initial symptomatic therapy for a presumed post-viral rash was ineffective. On examination, she had palpable purpura and erythematous lesions. Skin biopsy confirmed LCV. Rheumatology and dermatology were consulted. An extensive autoimmune and serologic workup for ANCA-associated vasculitis, Henoch-Schönlein purpura, cryoglobulinemia, and systemic lupus erythematosus was negative, and no systemic involvement was detected. High-dose corticosteroids were initiated, resulting in gradual improvement. Respiratory PCR testing was positive for C. pneumoniae. A diagnosis of LCV secondary to C. pneumoniae infection was made, and doxycycline was started, leading to near-complete resolution of the rash. Discussion Although C. pneumoniae is primarily a respiratory pathogen, several reports and reviews have highlighted its potential to induce immune-mediated skin manifestations. Compared with other atypical pneumonias, C. pneumoniae has been more frequently associated with cutaneous eruptions, including vasculitis, though this remains uncommon. The relationship between C. pneumoniae and LCV is rare but increasingly recognized. Published case reports describe LCV following respiratory infection with C. pneumoniae, occasionally accompanied by reactive arthritis or other autoimmune phenomena. Systematic reviews underscore its rarity, identifying only a few cases among numerous C. pneumoniae infections. Clinicians should therefore consider infectious etiologies, including respiratory pathogens, in unexplained vasculitis after infection. Conclusion This case underscores the importance of recognizing infection-associated vasculitis when rashes persist despite standard therapy. Early biopsy and multidisciplinary evaluation facilitate prompt diagnosis. Awareness of infectious triggers such as C. pneumoniae can guide targeted treatment and improve outcomes. This abstract is funded by: Not funded