Background: Patients admitted to the hospital frequently present with indication of infection, yet many presentations are ultimately attributable to noninfectious etiologies, such as acute MI, pericarditis, PE, pneumonia, drug-induced pneumonitis, pulmonary hemorrhage syndromes, COPD exacerbations, asymptomatic bacteriuria, alcohol withdrawal, delirium, autoimmune disease, drug reactions, postoperative inflammation, etc. Differentiating true infection from mimicking conditions is essential to avoid inappropriate antimicrobial use, prevent delays in necessary therapy, and improve clinical outcomes. Accurate acute bacterial–viral differentiation remains challenging, as traditional biomarkers and microbiologic testing are limited by variable sensitivity, specificity, and delays in obtaining actionable results. These challenges are amplified when inflammatory markers such as CRP are low despite an underlying bacterial process. Host response-based diagnostics, which assess the immune system rather than relying solely on pathogen detection, are emerging as valuable adjuncts. This work describes how a host-immune response assay (MeMed BV), measuring Tumor necrosis factor related apoptosis inducing ligand (TRAIL), the inflammatory chemokine interferon-gamma inducible protein of 10 kDa (IP-10), and C-reactive protein (CRP) and reports back an algorithm-calculated score, can support bacterial–viral differentiation reducing diagnostic ambiguity in complex patients during hospital admission.
Methods: We reviewed conventional diagnostic approaches alongside MeMed BV host-response assay, including analytical performance characteristics and integration into the clinical workflow. We highlight scenarios in which host-response profiling provided clarity when traditional markers were inconclusive. Case examples were explored to highlight clinical utility.
Results: The assay was incorporated into the workflow, with analytical performance and turnaround time meeting expectations. It reliably differentiated bacterial from viral infection in clinically complex presentations where traditional biomarkers were non-diagnostic. Case 1: 74 y/o M with hypoxia, inconclusive laboratory and imaging findings, yet MeMed BV produced a score of 99, indicating bacterial infection. This reduced diagnostic uncertainty and supported early treatment of aspiration pneumonitis. Case 2: 76 y/o F with abdominal pain, gastrointestinal distress, and SIRS, had a MeMed BV score of 17, consistent with viral infection, guiding the withholding of antibiotics to avoiding unnecessary treatment of non infective colitis and an asymptomatic UTI. Case 3: 73 y/o F with acute hypoxic respiratory failure and decompensated heart failure had overlapping signs of overload and possible infection. Despite nonspecific laboratory and image findings, the BV score was 92 supporting the diagnosis of superimposed bacterial pneumonia and prompting early IV antibiotics with diuresis. Across cases, the assay reduced ambiguity, supported timely treatment decisions, and may decrease unnecessary downstream testing and antibiotic exposure.
Conclusions: Real-world experience suggests that integrating host-response diagnostics may help resolve longstanding challenges in differentiating bacterial from viral infections in admitted patients. This approach has the potential to reduce unnecessary antibiotic use, improve diagnostic accuracy, and support timely evidence-based decision-making.