Remdesivir resistance in transplant recipients with persistent COVID-19

While measures to curb the spread of SARS-CoV-2, a pathogen that has claimed the lives of more than a million Americans, continue to ease in many parts of the United States, the risk of adverse outcomes related to infection in immunocompromised hosts remains substantial. In a recent meta-analysis that included nearly 12,000 solid organ transplant recipients, vaccination against COVID-19 elicited a humoral response that was significantly reduced compared to that of immunocompetent hosts.

Six months after transplant, the patient developed the new onset of malaise, fatigue, cough, and fever. On admission, nasopharyngeal RT-PCR was positive for SARS-CoV-2 with a cycle threshold of 27.1. Genomic sequencing identified the B.1.529 subvariant BA.1.1. Not requiring oxygen at that time, the patient received a five-day course of remdesivir, experienced improvement in symptomatology including defervescence, and was discharged.

24 days after the diagnosis of COVID-19, the patient was readmitted with worsening fatigue, cough, dyspnea, abdominal discomfort, and fever. Nasopharyngeal SARS-CoV-2 RT-PCR was again positive with a Ct of 24.4, and genomic sequencing identified Omicron BA.1.1. In the setting of a substantial oxygen requirement, the patient was treated with another five-day course of remdesivir and a ten-day course of dexamethasone.

110 days after COVID-19 diagnosis, the patient developed a new onset of dry cough and rhinorrhea. Nasopharyngeal RT-PCR was positive for SARS-CoV-2 with a Ct of 23.3 . RT-PCR for other respiratory pathogens was negative. Repeat RT-PCR one week later yielded a Ct of 22.6, and genomic sequencing at that time identified asynonymous mutation in RdRp at K890 . Providers monitored the patient’s mild symptoms, which gradually improved over the course of weeks.

Fourteen months after transplant, the patient developed malaise, shortness of breath, and cough. Nasopharyngeal PCR was positive for SARS-CoV-2, and in the setting of pulmonary infiltrates on x-ray and hypoxemia, the patient received a three-day course of remdesivir and a four-day course of baricitinib. SARS-CoV-2 genomic sequencing performed on day seven of illness identified aV792I mutation in RdRp .

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Long-term neuromuscular consequences of SARS-Cov-2 and their similarities with myalgic encephalomyelitis/chronic fatigue syndrome: results of the retrospective CoLGEM study - Journal of Translational MedicineBackground Patients with long-COVID often complain of continuous fatigue, myalgia, sleep problems, cognitive dysfunction, and post-exertional malaise. No data are available on EMG recording of evoked myopotentials (M-waves) or exercise-induced alterations in long-COVID patients, providing evidence of muscle membrane fatigue. Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) develops in more than half of patients after an infectious disease, particularly viral diseases. A large proportion (around 70%) of these patients have neuromuscular disorders with M-wave alterations during and after exercise. Our hypothesis was that M-wave alterations would be also found in long-COVID patients, in association with neuromuscular symptoms, similar to ME/CFS. Methods This retrospective observational ColGEM (Covid LonG Encéphalomyelite Myalgique) study compared 59 patients with long-COVID and 55 ME/CFS patients with a history of severe infection who presented before the COVID pandemic. All of these patients underwent the same protocol consisting of a questionnaire focusing on neural and neuromuscular disorders and M-wave recording in the rectus femoris muscle before, during, and 10 min after a progressive cycling exercise. Maximal handgrip strength (MHGS) and maximal exercise power were also measured. The frequency of symptoms and magnitude of M-wave changes in the two groups were compared using non-parametric and parametric tests. Results The frequency of fatigue, myalgia, sleep problems, cognitive dysfunction, and post-exertional malaise as well as the magnitude of exercise-induced M-wave alterations were the same in the two groups. By contrast, digestive problems were less present in long-COVID. M-wave alterations were greater in ME/CFS patients as in those with long-COVID when the highest muscle strength and highest exercise performance were measured. Conclusions These high clinical and biological similarities between long-COVID and ME/CFS support the hypothesis that S
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