A50-15 A Rare Case of Septic Shock and Atypical Hemolytic Uremic Syndrome Secondary to Capnocytophaga Canimorsus

Abstract Introduction (Rationale) Capnocytophaga canimorsus, a fastidious gram-negative bacterium from canine and feline oral flora, is known to cause fulminant sepsis especially in immunocompromised hosts. Thrombotic microangiopathy (TMA) triggered by C. canimorsus is exceedingly rare. We present a case of septic shock secondary to C. canimorsus that initially manifested as disseminated intravascular coagulation (DIC) and later evolved into a microangiopathic hemolytic anemia (MAHA) from atypical Hemolytic Uremic Syndrome (aHUS), underscoring the diagnostic and therapeutic challenges. Case Description A 66-year-old woman with chronic obstructive pulmonary disease and malnutrition presented with septic shock and multiorgan dysfunction. She was fluid resuscitated and started on broad spectrum antibiotics and vasopressors. Blood cultures grew C. canimorsus from an unclear source, but she reported exposure to dogs and cats at home. She denied vomiting or diarrhea prior to admission. Initial labs showed hemoglobin 13.7 mg/dl, platelets 39 k/uL, INR 3.2, aPTT 128 sec, fibrinogen 69 mg/dl, D-dimer 13 mg/L, LDH 1153 U/L, haptoglobin 10 mg/dl, consistent with DIC. Over the next few days, INR (1.1), platelets (62 k/uL), fibrinogen (251mg/dl), LDH and haptoglobin improved, consistent with resolution of DIC with improving sepsis. However, on hospital day 10, despite normalized coagulation factors and fibrinogen, she developed a new MAHA, with worsening renal failure requiring continuous renal replacement therapy (CRRT), recurrent thrombocytopenia (platelets 17 k/uL), elevated LDH (2,500 U/L), low haptoglobin (10 mg/dl), schistocytes on peripheral smear and severe limb necrosis. ADAMTS13 on day 11 was 35.4% (mildly low), making thrombotic thrombocytopenic purpura (TTP) unlikely, and plasmapheresis was not performed. Atypical HUS was suspected, and Eculizumab was initiated, leading to partial hematologic improvement (platelets 92 k/uL, haptoglobin 77mg/dl, LDH 344 U/L), but no recovery of renal function and patient remained on CRRT. The patient later developed progressive multiorgan failure and died. Discussion The case illustrates a transition from sepsis-associated DIC to complement-mediated TMA. Persistent hemolysis and thrombocytopenia despite DIC resolution suggested aHUS. ADAMTS13 activity 10% excluded TTP, and the absence of diarrheal illness ruled out typical HUS. C. canimorsus appears to have triggered complement activation, an association rarely reported. Eculizumab confirmed complement involvement but did not reverse renal injury. Recognizing complement-mediated coagulopathy in septic patients is critical for timely therapy. Conclusion Early identification of evolving coagulopathy and prompt initiation of complement inhibition can improve hematologic outcomes in C. canimorsus-associated aHUS, though outcomes may remain poor in critically ill patients. This abstract is funded by: None