P122 Diagnostic dilemma with lung cavities: a case of ANCA-associated vasculitis with concurrent <i>Actinomyces</i> infection

Abstract Introduction Cavitating lung lesions present a wide potential differential diagnosis, including infection, malignancy, infarction and autoimmune cause. With the presence of anti-neutrophil cytoplasmic antibodies (ANCA), this increases the suspicion of ANCA-associated vasculitis (AAV). When infection presents concurrently with AAV, early diagnosis can be challenging and can create diagnostic uncertainty and complex management dilemmas requiring careful multidisciplinary evaluation. Case description A 28-year-old male warehouse operator and smoker had a one-week history of pleuritic chest pain, a two-week history of sinus symptoms, epistaxis and haemoptysis, and a four-week history of night sweats and weight loss. Initial examination was unremarkable except mild throat erythema. Investigations revealed inflammatory response: leucocytosis, neutrophilia, mild eosinophilia, deranged liver function, elevated CRP and D-dimer. Renal function normal, urinalysis 3+ blood, culture negative. Glucose/HbA1c, Immunoglobulins, T-cell, NK-cell levels normal; HIV, hepatitis B and C negative. Chest X-ray and CT PA showed multiple bilateral cavitating lung lesions, some nodules and hilar lymphadenopathy, and no pulmonary embolism. c-ANCA pattern antibodies were positive with strong anti-Proteinase 3 (PR3) titre. Sputum culture including tuberculosis and quantiferon tested negative. CT sinuses showed sinusitis, polyposis and expansion without bony destruction. Treatment was initiated with prednisolone and rituximab for presumed AAV. Bronchoalveolar lavage (BAL) histology returned subsequently showing inflammatory response with filamentous bacillary colonies with central eosinophils, identified as Actinomyces spp., prompting cessation of steroids and commencement of high dose antibiotics. Renal biopsy showed no evidence of vasculitis. Lung histology reported mixed inflammation and fibrin with no granulomas or malignancy. CT of abdomen, pelvis and head reported enlarged spleen with diffuse low attenuation and both kidneys had wedge-shaped cortical hypodensities. CT angiogram aorta/coeliac showed no vascular abnormalities to support vasculitis, only changes suggestive of splenic and renal infarcts. Transthoracic echocardiogram was normal. The patient developed progressive lung lesions, rash, renal impairment, rising PR3 titre, DVT, persistent elevation of CRP and required supplemental oxygen. Repeat lung biopsy prior to anti-coagulation reported necrosis and acutely inflamed fibrotic stroma with some vessels showing fibrinoid necrosis and fibrin thrombi. Repeat renal biopsy not done prior to anti-coagulation. Immunosuppression was augmented with restarting steroids and addition of cyclophosphamide whilst high-dose antibiotics continued. Clinical parameters stabilised. Discussion This case exemplifies the diagnostic and management dilemma with lung cavities and AAV when infection co-presents. In this case, it was a rare subacute invasive bacterial infection caused by Actinomyces. The critical question during the diagnostic work up was whether this patient had AAV, disseminated actinomycosis infection or, as emerged, both. Pulmonary actinomycosis can occur when there is breakdown in tissue integrity, predisposed by dental issues, chronic lung disease, sinusitis and immunocompromise. There is a reported rise in Actinomyces spp.-associated infections, with peak incidence aged 30-50 years. Actinomycosis requires prolonged (6-12 months) high-dose antibiotics to clear, and haematological spread can result in disseminated micro-abscesses, with local tissue necrosis and granulomas. Some of these features overlap with potential clinical features of AAV. Adding to the complexity, ANCA antibodies can be positive in the presence of infection, and infection-induced AAV can occur. The BAL histology results were obtained prior to the start of immunosuppressive therapy for AAV and thought unlikely to be contamination from oral mucosa, given the eosinophilic material present with bacillus clusters. The clinical findings included strongly positive PR3-ANCA, systemic inflammatory response, and subsequent organ involvement including renal and splenic involvement. The relationship between the presence of AAV and Actinomyces infection is unclear. Three possibilities were considered: vasculitis predisposed the patient to opportunistic Actinomyces infection; Actinomyces infection triggered or drove the development of AAV, or both conditions developed independently as coincidental dual pathology. The patient’s clinical deterioration off steroids, coupled with evidence of progressive organ involvement, suggested vasculitis requiring treatment regardless of its relationship to infection. The multidisciplinary team ultimately concluded that the patient had both conditions requiring simultaneous management. This pragmatic approach acknowledged that definitive determination of their relationship was less important than addressing both pathological processes that posed considerable clinical risks. Key learning points • Pulmonary Actinomyces infection is a rare subacute opportunistic infection and can present similar features toAAV causing diagnostic dilemma. • The interaction between actinomycoses and AAV is uncertain. Lung cavities with ANCA antibodies may be associated with infection and screening for infection should always be carried out. • AAV and serious infections can present simultaneously and may need a concurrent treatment plan. • Negative microbiology screening does not exclude infection, as demonstrated by subsequent identification of Actinomyces despite extensive work up. • Multiple sites and repeat tissue sampling for analysis may be necessary to establish diagnosis. • Interdisciplinary MDT management of such complex presentations is essential. • Clinical practice may demand therapeutic intervention based on probability and risk assessment without absolute certainty.