Background The COVID-19 pandemic has led to significant reductions in transplantation, motivated in part by concerns of disproportionately more severe disease among solid organ transplant (SOT) recipients. However, clinical features, outcomes, and predictors of mortality in SOT recipients are not well-described. Methods We performed a multi-center cohort study of SOT recipients with laboratory-confirmed COVID-19. Data were collected using standardized intake and 28-day follow-up electronic case report forms. Multivariable logistic regression was used to identify risk factors for the primary endpoint, 28-day mortality, among hospitalized patients. Results Four hundred eighty-two SOT recipients from >50 transplant centers were included: 318 (66%) kidney or kidney/pancreas, 73 (15.1%) liver, 57 (11.8%) heart, and 30 (6.2%) lung. Median age was 58 (IQR 46-57), median time post-transplant was 5 years (IQR 2-10), 61% were male, and 92% had ≥1 underlying comorbidity. Among those hospitalized (376 [78%]), 117 (31%) required mechanical ventilation, and 77 (20.5%) died by 28 days after diagnosis. Specific underlying comorbidities (age >65 [aOR 3.0, 95%CI 1.7-5.5, p<0.001], congestive heart failure [aOR 3.2, 95%CI 1.4-7.0, p=0.004], chronic lung disease [aOR 2.5, 95%CI 1.2-5.2, p=0.018], obesity [aOR 1.9, 95% CI 1.0-3.4, p=0.039]) and presenting findings (lymphopenia [aOR 1.9, 95%CI 1.1-3.5, p=0.033], abnormal chest imaging [aOR 2.9, 95%CI 1.1-7.5, p=0.027]) were independently associated with mortality. Multiple measures of immunosuppression intensity were not associated with mortality. Conclusions Mortality among SOT recipients hospitalized for COVID-19 was 20.5%. Age and underlying comorbidities rather than immunosuppression intensity-related measures were major drivers of mortality.

There have been multiple descriptions of seizures during the acute infectious period in patients with COVID-19. However, there have been no reports of status epilepticus after recovery from COVID-19 infection. Herein, we discuss a patient with refractory status epilepticus 6 weeks after initial infection with COVID-19. Extensive workup demonstrated elevated inflammatory markers, recurrence of a positive nasopharyngeal SARS-CoV-2 polymerase chain reaction, and hippocampal atrophy. Postinfectious inflammation may have triggered refractory status epilepticus in a manner similar to the multisystemic inflammatory syndrome observed in children after COVID-19.

Data describing the clinical progression of coronavirus disease 2019 (COVID‐19) in transplant recipients are limited. In New York City during the surge in COVID‐19 cases, a systematic approach to monitoring and triaging immunocompromised transplant patients was required in the context of strained healthcare resources, limited outpatient testing, and heightened hospital exposure risks. Public health guidance at the onset of the COVID‐19 outbreak recommended outpatient monitoring of mildly symptomatic patients without specific recommendations for special populations such as transplant recipients. We developed and implemented a systematic monitoring algorithm for kidney transplant recipients at our transplant center who reported mild symptoms suggestive of COVID‐19. We describe the outcomes of the first 44 patients monitored through this algorithm. A total of 44 kidney transplant recipients thought to be symptomatic for COVID‐19 disease were followed for a minimum of 14 days. The majority of mildly symptomatic patients (34/44) had clinical progression of disease and were referred to the emergency department where they all tested PCR positive and required hospitalization. More than half of these patients presented with hypoxia requiring supplemental oxygen, 39% were intubated within 48 hours, and 53% developed acute kidney injury but did not require dialysis. There were 6 deaths. During surge outbreaks, kidney transplant patients with even mild symptoms have a high likelihood of COVID‐19 disease and most will worsen requiring hospitalization for supportive measures. Earlier outpatient testing and hospitalization may improve COVID‐19 outcomes among transplant recipients.

f This case series highlights our experience with use of the Fungitell assay for quantifying (1,3)-␤-D-glucan in cerebrospinal fluid during the current U.S. outbreak of fungal meningitis related to contaminated methylprednisolone acetate. This test may prove a useful adjunct in diagnosis and management of exposed patients.(1,3)-␤-D-glucan (BG) is found in cell walls of multiple fungi. Its detection in serum assists in diagnosis of invasive fungal infections (1). Recently, diagnostic challenge has arisen in the fungal meningitis outbreak associated with exposure to contaminated epidural steroid injections (2). Diagnosis in this setting has been established by culture of cerebrospinal fluid (CSF) and/or detection using a pan-fungal PCR assay performed by the Centers for Disease Control (CDC). However, these tests have not always been positive in suspected cases (3). One early study has demonstrated the proof of concept of using CSF BG detection in diagnosis of fungal central nervous system infection in an experimental hematogenous Candida meningoencephalitis model (4). Here we report our experience with CSF BG measurement in 5 individuals from Johns Hopkins Hospital and Indiana University Hospital who were exposed to potentially contaminated drugs. Cases were diagnosed and managed according to CDC guidelines. BG was tested at Beacon Diagnostics Laboratory (East Falmouth, MA) using the Fungitell assay. Information was obtained by chart review with approval from the Johns Hopkins Institutional Review Board.The first case was a 55-year-old woman who developed headaches, blurred vision, and injection site pain 1 week after lumbar epidural injection with potentially contaminated methylprednisolone and was admitted 35 days after symptom onset when the outbreak was recognized. CSF showed 30 white blood cells (WBCs)/mm 3 and normal glucose and protein; no opening pressure was recorded. Intravenous voriconazole was initiated, but symptoms continued despite troughs of 2 to 3 g/ml. Repeat lumbar puncture (LP) showed opening pressure of 42 cm H 2 O, 974 WBC/mm 3 (56% neutrophils, 16% lymphocytes, 21% monocytes), 1,000 red blood cells (RBCs)/mm 3 , normal glucose, and 93 mg/dl protein, with a negative culture. CSF PCR performed by the CDC was negative. With serial LPs for persistent headache and elevated opening pressures and voriconazole increase to maintain troughs of 3 to 5 g/ml, her symptoms resolved. CSF fungal cultures from postinjection days 57, 69, and 73 were negative. CSF BG samples sent on postinjection days 57 and 73 were positive at 2,396 and 701 pg/ml, respectively (Table 1).The second case was a 37-year-old man who underwent lumbar epidural injection with potentially contaminated methylprednisolone and developed a headache several days later. Thirteen days after the injection he started oral voriconazole. His symptoms did not improve, and LP 2 weeks later showed 5 WBCs/mm 3 ( Table 1). PCR performed by the CDC and fungal cultures were negative. Magnetic resonance imaging (MRI) of the brain showed a small intrapa...