Abstract Hypervirulent Klebsiella pneumoniae (hvKp) is an emerging pathogen causing invasive, community-acquired infections with devastating metastatic potential. The resulting Klebsiella Liver Abscess Syndrome (KLAS) may trigger a systemic inflammatory cascade clinically and biochemically indistinguishable from hemophagocytic lymphohistiocytosis (HLH). This case highlights the need for prompt source control and antibiotics, as any delay can be catastrophic. A 33 year old man from Ghana with poorly controlled type 2 diabetes presented with one week of high grade fevers, malaise, anorexia, and progressive jaundice. On admission, he was febrile to 39.3 degree C, tachycardic, and icteric, with right upper-quadrant tenderness. Initial studies showed thrombocytopenia, direct hyperbilirubinemia, and ferritin more than 10 000 ng/mL. The soluble IL2 receptor was elevated at 4420 U/mL, raising concern for secondary HLH, and oncology recommended bone-marrow evaluation. Contrast-enhanced CT of the abdomen revealed multiple rim-enhancing hepatic abscesses with septic thrombophlebitis of the middle hepatic vein (Figure 1), redirecting suspicion toward invasive infection. Blood cultures grew a hypermucoviscous strain of K. pneumoniae, confirming hvKp KLAS. On hospital day three, he developed sudden, painless left-eye blindness. Ophthalmology confirmed complete exudative retinal detachment without vitritis (Figure 1). Intravitreal antibiotics were deferred, and systemic therapy continued. Despite treatment, vision loss was permanent due to retinal ischemia. Within 24 hours, he developed hypoxemic respiratory failure. Chest CT showed bilateral septic emboli, ground-glass opacities, and small pleural effusions. He was transferred to the ICU for mechanical ventilation. Management included meropenem, image-guided abscess drainage, anticoagulation for hepatic-vein thrombosis, and meticulous glycemic and ventilatory support. Over two weeks, hemodynamics improved, but blindness persisted. This case illustrates how disseminated hvKp infection can mimic HLH. The patient met several HLH-2004 criteria fulfilling at least five of eight elements before marrow evaluation: fever, cytopenias, hyperferritinemia, elevated soluble IL-2 receptor, and hepatic dysfunction. The elevated ferritin and IL-2 receptor reflected an extreme cytokine response to hvKp rather than malignancy-associated HLH. Recognition of infection through imaging and cultures prevented inappropriate immunosuppression. The case revealed the protean nature of hvKp infection, capable of causing rare metastatic complications like exudative retinal detachment and septic pulmonary emboli through hematogenous dissemination in diabetic hosts. Early differentiation between infection-associated hyperinflammation and true HLH is critical. Prompt imaging, microbiologic confirmation, and source control remain key to preventing irreversible outcomes such as blindness and respiratory failure. This abstract is funded by: None
Ahsan et al. (Fri,) studied this question.