ABSTRACT
Strongyloides stercoralis is a soil-transmitted helminth endemic to tropical and subtropical regions and can be acquired due to parasite penetration through the skin. It can remain dormant in the gastrointestinal system for decades after the primary infection. In immunocompromised patients, this parasite can cause autoinfection with progression to hyperinfection syndrome. Here we report a unique case of pulmonary strongyloidiasis in a 32-year-old female, originally from Guatemala, with a significant clinical history of Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia diagnosed in 2019. The patient is status post chemotherapy with tyrosine kinase inhibitor plus hyper-CVAD regimen (Cyclophosphamide, Vincristine sulfate, Doxorubicin hydrochloride (Adriamycin), and Dexamethasone). History of drug-induced hyperglycemia and obesity was also noted. Her current chief complaint included dyspnea, tachycardia, and chest pain. Chest computerized tomography (CT) scan showed diffuse interstitial pulmonary edema with septal thickening, scattered ground-glass opacities, and small pericardial effusion. Due to normal ejection fraction, the differential diagnosis included non-cardiogenic pulmonary edema, pneumonitis secondary to chemotoxicity, and infection. She rapidly progressed to acute hypoxic respiratory failure, and a bronchoalveolar lavage study revealed numerous larvae consistent with Strongyloides hyperinfection. Further workup revealed eosinophilia with negative Strongyloides IgG antibody. Given the rarity of this infection in the United States and the patient's place of birth, acquired latent Strongyloides infection is favored as the initial source of infection. The reactivation of the infection process was most likely secondary to her chemotherapy treatment. Strongyloides hyperinfection diagnosis can be challenging to establish and entails a high level of suspicion. Cytology evaluation is an essential factor for diagnosis.
ABSTRACT
OBJECTIVES: With the ongoing emergence of SARS-CoV-2 variants and potential to evade vaccine-induced neutralisation, understanding the magnitude and breadth of vaccine-induced T-cell immunity will be critical for the ongoing optimisation of vaccine approaches. Strategies that provide a rapid and easily translatable means of assessing virus-specific T-cell responses provide an opportunity to monitor the impact of vaccine rollouts in the community. In this study, we assessed whether our recently developed SARS-CoV-2 whole-blood assay could be used effectively to analyse T-cell responses following vaccination. METHODS: Following a median of 15 days after the first dose of the ChAdOx1-S (AstraZeneca®) vaccine, peripheral blood was isolated from 58 participants. Blood was incubated overnight with an overlapping set of spike protein peptides and assessed for cytokine production using a cytometric bead array. RESULTS: The majority of vaccine recipients (51/58) generated a T helper 1 response (IFN-γ and/or IL-2) following a single dose of ChAdOx1-S. The magnitude of the IFN-γ and IL-2 response strongly correlated in vaccine recipients. While the production of other cytokines was evident in individuals who did not generate IFN-γ and IL-2, they showed no correlation in magnitude, nor did we see a correlation between sex or age and the magnitude of the response. CONCLUSIONS: The whole-blood cytokine assay provides a rapid approach to assessing T-cell immunity against SARS-CoV-2 in vaccine recipients. While the majority of participants generated a robust SARS-CoV-2-specific T-cell response following their first dose, some did not, demonstrating the likely importance of the booster dose in improving T-cell immunity.