The patient’s story began innocuously. He had been treated with rabbit anti-thymocyte globulin and cyclosporine between June and October 2024 for marrow hypoplasia, leaving him profoundly immunosuppressed and neutropenic, with absolute neutrophil counts hovering between 320 and 390 cells per microliter. A non-enhanced chest computed tomography scan performed at an outside facility showed consolidation in the right lung, and he was given empiric ciprofloxacin for presumed pneumonia. Notably, he had no fever and no respiratory symptoms at that stage, and laboratory markers including carcinoembryonic antigen, neuron-specific enolase, beta-D-glucan and Aspergillus antigen all came back unremarkable. In an immunocompromised host, however, consolidation is usually treated as infection until proven otherwise, and the initial workup proceeded along those lines.

The turning point came on Day 14, when a repeat non-enhanced chest CT showed marked worsening of the right lower lobe lesion, with a mixture of ground-glass opacity and consolidation, a new pleural effusion, and scattered nodules surrounded by halo signs. That radiologic pattern, in which a nodule is ringed by a rim of ground-glass attenuation, is classically associated with invasive pulmonary aspergillosis, although mucormycosis could not be excluded. A cough developed around the same time and a single fever of 38.1 degrees Celsius was recorded at admission, but the patient never required supplemental oxygen. Bronchoscopy on Day 15 revealed no endobronchial lesions, and the bronchoalveolar lavage fluid from the right anterior basal segment was xanthochromic, a yellowish discoloration that, in retrospect, signaled occult alveolar hemorrhage linked to infarction rather than the cloudy return typical of pneumonia.

Every microbiologic test came back negative. Bacterial and fungal cultures, galactomannan assays and viral polymerase chain reaction panels were all sterile, and a transbronchial lung biopsy showed only focal organizing pneumonia without fungal elements. Nevertheless, because the parenchymal disease was worsening, the clinical team initiated liposomal amphotericin B and piperacillin-tazobactam, a broad-spectrum antifungal and antibacterial combination. The lung lesion failed to improve. This disconnect between aggressive antimicrobial therapy and persistent radiologic disease should have been the first clear signal that the working diagnosis was wrong, and it set the stage for a more careful look at the pulmonary vasculature.

That look came indirectly. Concerned about the patient’s coexisting chronic kidney disease, clinicians obtained another non-enhanced chest CT on Day 20, which revealed a dilated main pulmonary artery, enlargement of the right-sided cardiac chambers and a pericardial effusion, a triad suggestive of pulmonary hypertension. A contrast-enhanced chest CT on Day 21 then delivered the answer: a low-attenuation filling defect in the right interlobar and lower lobar pulmonary arteries, with associated infarction of the lung tissue downstream. Anticoagulation was started immediately. Because the scan had not been performed with a dedicated pulmonary embolism protocol, CT pulmonary angiography was repeated on Day 27, showing that the filling defect persisted after a week of anticoagulation and had extended into the lobar branches. Its unilateral, expansile appearance raised a new and alarming possibility: pulmonary artery sarcoma, an exceptionally rare malignancy with an estimated incidence of only 0.001 to 0.03 percent.

Distinguishing a chronic organized thrombus from an intraluminal sarcoma is one of the classic dilemmas in pulmonary vascular imaging. Chronic thromboembolic pulmonary hypertension typically produces vessel narrowing or intraluminal webs, whereas sarcoma tends to appear as an expansile, lobulated mass that distends the artery. In this case, fluorodeoxyglucose positron emission tomography on Day 29 showed only mildly heterogeneous uptake within the lesion, with a maximum standardized uptake value of 2.9, a level that favored thrombus over tumor. Endobronchial ultrasound-guided transbronchial needle aspiration of the right lower lobe pulmonary artery, a technique highlighted in the report as a safe route for tissue acquisition, yielded whitish necrotic cores. Pathology described predominantly thrombotic material with only a few atypical cells, insufficient to exclude malignancy. Right heart catheterization confirmed precapillary pulmonary hypertension, and angiography demonstrated total occlusion of the right lower lobe pulmonary artery.

With the lesion persisting after nearly a month of anticoagulation and malignancy still on the differential, the team planned a pulmonary endarterectomy, a procedure that could serve as both treatment and definitive biopsy. Because the patient remained clinically stable without oxygen requirement or worsening breathlessness, the operation was scheduled electively. While awaiting surgery, however, his dyspnea gradually worsened and the pleural effusion grew, prompting readmission and an earlier operation on Day 87. Surgeons found extensive material filling the right pulmonary artery and dissected it distally into the lobar branches, consistent with level III disease in the UCSD surgical classification of endarterectomy findings. The decisive result came from histopathology: Brown and Brenn staining revealed Gram-positive cocci within the organizing thrombus, confirming a septic pulmonary artery thrombus. The patient later recalled a remote dental implant infection, a plausible source of the bacteremia that had seeded the vessel. He completed four weeks of ceftriaxone, and after an urgent re-exploration for postoperative bleeding, he recovered without further surgical complications.

The case is remarkable for what it lacked as much as for what it showed. A septic thrombus inside a major pulmonary artery would ordinarily be expected to produce overt sepsis or signs of infective endocarditis, yet this patient had essentially none of the classic systemic features. The report notes that septic pulmonary embolism can present with attenuated systemic manifestations, particularly in patients with prior antimicrobial exposure or immunosuppression, both of which applied here. Antibiotics given for the presumed pneumonia may have partially suppressed the inflammatory response, while the underlying immunosuppressive therapy blunted fever and other warning signs. The result was a vascular infection smoldering silently for weeks, masquerading first as pneumonia and then as an aggressive fungal process, and only unmasked when imaging of the pulmonary arteries was finally performed with contrast.

The authors distill several lessons that extend well beyond this single patient. Pulmonary consolidation that follows an atypical course or fails to respond to appropriate antimicrobials should prompt consideration of pulmonary infarction, and dedicated CT pulmonary angiography should be obtained early once a vascular etiology is suspected, rather than relying on non-enhanced or non-dedicated scans. A unilateral pulmonary artery filling defect that persists despite adequate anticoagulation, especially when accompanied by pulmonary hypertension, warrants evaluation for chronic thromboembolic disease and pulmonary artery malignancy. Metabolic imaging with FDG PET-CT and minimally invasive sampling through EBUS-guided needle aspiration can provide useful clues, but as this case demonstrates, they may remain non-diagnostic, and surgical pathology or endarterectomy may ultimately be required to settle the question.

For clinicians caring for the growing population of immunocompromised patients, the message is a sobering one. The xanthochromic bronchoalveolar lavage fluid, the early CT signs of pulmonary hypertension, and the relentless progression despite broad-spectrum therapy were all, in hindsight, pointing toward a vascular catastrophe rather than an infection. Recognizing those signals sooner could have shortened a diagnostic odyssey that stretched across nearly three months from first scan to definitive surgery. Septic organizing thrombus of the pulmonary artery remains a rare diagnosis, but as this case makes clear, it belongs on the differential for any immunocompromised patient whose lung lesion refuses to behave like pneumonia, and whose arteries tell a story the parenchyma has been hiding all along.

Subject of Research: Septic pulmonary artery thrombus causing pulmonary infarction in an immunocompromised patient

Article Title: Unilateral Pulmonary Artery Lesion in an Immunocompromised Patient

Article References: Lee, S., Lee, K. S., Jeong, D. Y., Lee, B., Lee, J., Jeong, D. S., Chang, S.-A., & Shin, S. H. (2026). Unilateral Pulmonary Artery Lesion in an Immunocompromised Patient. Respirology Case Reports, 14(10), Article e70778. https://doi.org/10.1002/rcr2.70778

Image Credits: AI Generated

DOI: 10.1002/rcr2.70778

Keywords: pulmonary artery thrombus, pulmonary infarction, immunocompromised, myelodysplastic syndrome, pulmonary hypertension, pulmonary endarterectomy, CT pulmonary angiography, FDG PET-CT, EBUS-TBNA, septic pulmonary embolism, pulmonary artery sarcoma, chronic thromboembolic disease