Abstract Background Candida parapsilosis is a leading cause of candidemia in hospitalized patients, typically linked to central venous catheters, parenteral nutrition, and overt immunosuppression. Pulmonary tuberculosis (TB), while not classically associated with fungal infection, can disrupt systemic immunity through immunomodulatory effects. We present a rare case of C. parapsilosis fungemia in a patient with cavitary TB and no traditional risk factors—other than poorly controlled diabetes mellitus—highlighting a convergence of metabolic and infectious susceptibility. Case Presentation A 75-year-old man with uncontrolled type 2 diabetes mellitus (HbA1c 11.7%), hypertension, and hyperlipidemia presented with three weeks of productive cough, hemoptysis, dyspnea, and weight loss. Chest CT revealed bilateral upper lobe infiltrates with a large right upper lobe cavity. He was AFB smear 3+ and PCR-positive for Mycobacterium tuberculosis. Initial routine and fungal sputum cultures were negative. HIV and hepatitis panels, galactomannan, and β-D-glucan were also negative. He was started on standard anti-TB therapy. Ten days into hospitalization, he developed fever, chills, and leukocytosis. Blood cultures grew C. parapsilosis. He had no central venous catheter, parenteral nutrition, or recent instrumentation. He was treated with intravenous micafungin for seven days followed by oral fluconazole for seven days, with clearance of fungemia. Repeat blood cultures were negative, and he was discharged in stable condition. Discussion This case illustrates a rare dual infection—Mycobacterium tuberculosis and Candida parapsilosis—in a patient without classical immunosuppression or iatrogenic risk factors. Tuberculosis impairs cellular immunity via Th1 suppression and IL-10-mediated modulation, while chronic hyperglycemia disrupts neutrophil chemotaxis, phagocytosis, and mucosal barrier function. Together, these mechanisms may create an immune environment permissive to opportunistic fungal infections, even in the absence of HIV or invasive devices. We propose that poorly controlled diabetes may represent a distinct, underrecognized form of functional immunodeficiency. In the setting of chronic hyperglycemia and persistent infection, host defenses may be sufficiently impaired to permit opportunistic co-infections typically seen only in overtly immunocompromised individuals. To characterize this emerging clinical pattern, we introduce the provisional term Diabetes-Associated Immunodeficiency (DAI)—a state of hyperglycemia-induced immune susceptibility in individuals otherwise considered immunocompetent. While precise thresholds remain undefined, the association between hyperglycemia and opportunistic infection in this case highlights the need for systematic study. Analogous to diabetic nephropathy or retinopathy, DAI may represent a cumulative phenomenon, with immunologic risk increasing as metabolic control deteriorates. Further investigation is needed to define the immunopathologic basis of DAI and identify candidate biomarkers for risk stratification. This abstract is funded by: None
Rose et al. (Fri,) studied this question.