Nasal Septal Cartilage as Anterior Cap-Graft for Open Tracheoplasty in Cases for Laryngotracheal Stenosis: Our Initial Experience.

The aim of our study is to analyze the efficacy of nasal septal cartilage as cap-graft in laryngo-tracheoplasty in cases of Laryngotracheal stenosis. This was a prospective observational study carried out at a tertiary care hospital from March 2020 to March 2023. Total 8 patients who underwent laryngo-tracheoplasty using nasal septal cartilage as anterior Cap-graft were included in the study. Detailed history and clinical evaluation followed by diagnostic Flexible Fiber-optic Laryngoscopy and radiological investigations were done for all patients with post operative follow up for at least 1 year. Our study had maximum patients in age group of 11-30 years with male predominance, unknown compound ingestion being most common cause of intubation which was followed by tracheostomy. All patients had Cotton Mayer Grade III or IV subglottic stenosis. Out of 8 patients, 5 patients are decannulated, 1 patients still have T-tube in-situ whereas 2 patients didn't tolerate decannulation and required re-exploration. No donor site complication was seen during the study period. Nasal septal cartilage is a viable option for being used as anterior cap graft in laryngo-tracheoplasty. It can be a game changer, as can be done by E.N.T surgeon himself. No separate learning skills are required. It's cosmetically better with minimal complications; compared to life threatening complications like pneumothorax on using costal cartilage. Laryngeal framework is preserved as opposed to thyroid alar cartilage graft. Faster healing along with better postoperative donor site recovery are significant advantages.

Analysis of Artificial Intelligence-Based Approaches Applied to Non-Invasive Imaging for Early Detection of Melanoma: A Systematic Review.

BACKGROUND: Melanoma, the deadliest form of skin cancer, poses a significant public health challenge worldwide. Early detection is crucial for improved patient outcomes. Non-invasive skin imaging techniques allow for improved diagnostic accuracy; however, their use is often limited due to the need for skilled practitioners trained to interpret images in a standardized fashion. Recent innovations in artificial intelligence (AI)-based techniques for skin lesion image interpretation show potential for the use of AI in the early detection of melanoma. OBJECTIVE: The aim of this study was to evaluate the current state of AI-based techniques used in combination with non-invasive diagnostic imaging modalities including reflectance confocal microscopy (RCM), optical coherence tomography (OCT), and dermoscopy. We also aimed to determine whether the application of AI-based techniques can lead to improved diagnostic accuracy of melanoma. METHODS: A systematic search was conducted via the Medline/PubMed, Cochrane, and Embase databases for eligible publications between 2018 and 2022. Screening methods adhered to the 2020 version of the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Included studies utilized AI-based algorithms for melanoma detection and directly addressed the review objectives. RESULTS: We retrieved 40 papers amongst the three databases. All studies directly comparing the performance of AI-based techniques with dermatologists reported the superior or equivalent performance of AI-based techniques in improving the detection of melanoma. In studies directly comparing algorithm performance on dermoscopy images to dermatologists, AI-based algorithms achieved a higher ROC (>80%) in the detection of melanoma. In these comparative studies using dermoscopic images, the mean algorithm sensitivity was 83.01% and the mean algorithm specificity was 85.58%. Studies evaluating machine learning in conjunction with OCT boasted accuracy of 95%, while studies evaluating RCM reported a mean accuracy rate of 82.72%. CONCLUSIONS: Our results demonstrate the robust potential of AI-based techniques to improve diagnostic accuracy and patient outcomes through the early identification of melanoma. Further studies are needed to assess the generalizability of these AI-based techniques across different populations and skin types, improve standardization in image processing, and further compare the performance of AI-based techniques with board-certified dermatologists to evaluate clinical applicability.

Intraocular Lens Power Calculations in Keratoconus Eyes Comparing Keratometry, Total Keratometry, and Newer Formulae.

PURPOSE: To compare the utility of keratometry vs total keratometry (TK) for intraocular lens power calculations in eyes with keratoconus (KCN) using KCN and non-KCN formulae. DESIGN: Retrospective cohort study. METHODS: This study was conducted at 2 academic centers and included 87 eyes in 67 patients who underwent cataract surgery between 2019 and 2021. Biometry measurements were obtained using a swept-source optical coherence tomography biometer (IOL Master 700). Refractive prediction errors, including root mean square error (RMSE), were calculated for 13 formulae. These included 4 classical formulae (Haigis, Hoffer Q, Holladay 1 [H1], and SRK/T), 5 new formulae (NF) (Barrett Universal II [BU2], Cooke K6, EVO 2.0, Kane, and Pearl-DGS), 3 KCN formulae (BU2 KCN: M-PCA, BU2 KCN: P-PCA, and Kane KCN), and H1 with equivalent keratometry reading values (H1-EKR). Formulae were ranked by RMSE. Friedman analysis of variance with post hoc analysis and H-testing was used for statistical significance testing. RESULTS: KCN formulae had the lowest RMSEs in all eyes, and BU2 KCN:M-PCA performed the best among KCN formulae in all subgroups. In eyes with severe KCN, if TK values are unavailable, the BU2 KCN: P-PCA performed better than the top-ranked non-KCN formula (SRK/T). In eyes with nonsevere KCN, if TK values are unavailable, EVO 2.0 K was statistically superior to the next competitor (Kane K). H1-EKR had the highest RMSE. CONCLUSIONS: KCN formulae and TK are useful for intraocular lens power calculations in KCN eyes, especially in eyes with severe KCN. The BU2 KCN: M-PCA using TK values performed best for eyes with all severities of KCN. For eyes with nonsevere KCN, the EVO 2.0 TK or K can also be used.

Papuloerythroderma of Ofuji in a Young Man.

Papuloerythroderma of Ofuji (PEO) is a rare skin disorder characterized by a distinctive pattern of pruritic, flat-topped, erythematous papules which coalesce into an erythroderma-like eruption with classic sparing of the skin folds. Although the pathogenesis of this condition is incompletely understood, previous reports have suggested a notable link between PEO and various forms of malignancy and immunocompromised states. Here, we report a case of a healthy young male with no comorbidities who presented with the classical features of PEO that responded well to combination therapy comprised of topical corticosteroids and phototherapy.

Non-insulinoma pancreatogenous hypoglycemia syndrome due to nesidioblastosis following bariatric Roux-en-Y gastric bypass.

A 56-year-old woman with past medical history significant for bariatric Roux-en-Y gastric bypass 3 years prior presented for evaluation of an 8-month history of severe hypoglycemia relieved by intake of carbohydrates associated with syncopal episodes. Inpatient workup revealed endogenous hyperinsulinemia concerning for insulinoma vs. nesidioblastosis. She successfully underwent pancreaticoduodenectomy (Whipple procedure), and pathology report confirmed scattered low-grade intraepithelial neoplasia within the pancreatic parenchyma consistent with nesidioblastosis. The patient has had satisfactory control of glucose levels 30 days out from surgery.

Signaling through the IL-6-STAT3 Pathway Promotes Proteolytically-Active Macrophage Accumulation Necessary for Development of Small AAA.

INTRODUCTION: Elevated interleukin-6 (IL-6) plasma levels have been associated with abdominal aortic aneurysm (AAA), but whether this cytokine plays a causative role in the degenerative remodeling or represents an effect from the inflammatory cascades initiated by infiltrating leukocytes remained unclear. This project aims to demonstrate that within the aortic wall, signaling from IL-6 through the STAT3 transcription factor is necessary for infiltration of proteolytically-active macrophages and development of small AAA. METHODS: Following measurement of baseline infrarenal aortic diameter (AoD, digital microscopy), C57Bl/6 and IL-6 knockout (IL-6KO) mice underwent AAA induction by application of peri-adventitial CaCl2 (0.5 M) +/- implantation of an osmotic mini-pump delivering IL-6 (4.36 µg/kg/day over 21 days). At the terminal procedure, AoDs were measured by digital microscopy and aortas harvested for immunoblot (pSTAT3/STAT3), matrix metalloproteinase (MMP) quantification, or flow cytometric analysis of macrophage content. Plasma was collected for cytokine analysis. RESULTS: IL-6 infusion significantly increased the plasma IL-6 levels in C57Bl/6 and IL-6KO animals. The C57Bl/6 + CaCl2 group developed AAA (AoD >50% above baseline) but IL-6KO + CaCl2 did not. In the IL-6KO + IL-6+CaCl2 group, AAA developed to match that of C57Bl/6 + CaCl2 mice. STAT3 activity was significantly increased in animals with advanced stages of dilation (>40% from baseline), compared to those with ectasia (≤25%). Although cytokine profiles did not support T-cells or neutrophils as being active contributors in this stage of aortic remodeling, changes in the profile of elaborated MMPs suggested macrophage activity with a trend toward alternatively activated pathways. Flow cytometry confirmed significantly increased macrophage abundance specifically in animals with upregulated STAT3 activity and advanced aortic dilation. CONCLUSION: In this murine model of AAA, progressive dilation to development of true AAA was only accomplished when IL-6 signaling upregulated STAT3 activity to effect accumulation of proteolytically-active macrophages. This pathway warrants further investigation to identify potential therapeutic avenues to abrogate growth of small AAA.

Validating the Clinical Value of Temporal Artery Biopsy.

BACKGROUND: Giant cell arteritis (GCA) is a potentially devastating disease that may require treatment with high-dose steroids. Traditionally, diagnosis requires patients to meet at least 3 of 5 clinical criteria, one of which is a positive temporal artery biopsy (TAB). Vascular surgeons are often asked to perform TAB though it is not necessarily required for diagnosis or management. This study aimed to determine if TAB results altered management of patients with a concern for GCA by changing steroid use postoperatively in our health care system. METHODS: A retrospective review at a single-center tertiary care hospital was performed between 2007 and 2018. The inclusion criteria were patients greater than 18 years old with complete steroid treatment records who underwent a temporal artery biopsy due to concern for GCA. Steroid use and duration of treatment both pre- and post-operative were collected and analyzed. RESULTS: Eighty-three of 117 cases reviewed met inclusion criteria. Ninety-one percent (76) of patients had a negative biopsy. Twenty-nine percent (23) of negative biopsies met criteria for GCA prior to biopsy. Of those with a negative biopsy, steroids were continued in 68% (52) of patients after 30 days, 49% (37) after 90 days and 45% (34) after 180 days. Steroids were never started in 11% (6). One patient with a positive biopsy was discontinued on steroids due to intolerance. There was no statistically significant difference in duration of steroids between those with a positive and negative biopsy (average 610 and 787 days respectively; P = 0.682). Average follow up was 33 months. DISCUSSION: The duration of steroid use for patients with concern for GCA was not found to be altered by the performance of a TAB at our institution. Given the extremely low yield and absence of impact on steroid duration, TAB is not a useful diagnostic test at our institution. Similar reviews are recommended to determine the utility of TAB at other institutions that may differ in patient population or prescribing practices.

Outcomes of Over 1000 Heart Transplants Using Hepatitis C-Positive Donors in the Modern Era.

BACKGROUND: Advances in hepatitis C virus (HCV) treatment and the ongoing opioid epidemic have made HCV-positive donors increasingly available for heart transplantation (HT). This analysis reports outcomes of over 1000 HCV-positive HTs in the United States in the modern era. METHODS: The United Network of Organ Sharing registry was used to identify HTs between 2015 and 2021. Recipients were grouped by donor HCV status and by nucleic acid amplification test (NAT) positivity. The primary outcome was 1-year mortality, and secondary outcomes included 3-year mortality. A subanalysis compared HCV-positive HT outcomes between NAT-positive and NAT-negative donors. Risk adjustment was performed using Cox regression. Kaplan-Meier analysis was used to estimate survival. RESULTS: The frequency of HCV-positive HT increased from 0.12% of HTs in 2015 to 12.9% in 2021 (P < .001). Of 16,648 HTs, 1170 (7.0%) used an organ from an HCV-positive donor. Recipients of HCV-positive organs were more likely to be HCV seropositive, older, and White. Unadjusted 1- and 3-year survival rates were not significantly different between recipients of HCV-negative and HCV-positive organs. After risk adjustment HCV-positive donor status was not associated with an elevated risk for 1-year (hazard ratio, 0.92; 95% CI, 0.71-1.19; P = .518) or 3-year mortality. Among HCV-positive HTs 772 (61.7%) were NAT positive. After risk adjustment NAT positivity did not impact 1-year mortality. CONCLUSIONS: The proportion of HCV-positive HTs has increased over 100-fold in recent years. This analysis of the US experience demonstrates that recipients of HCV-positive hearts, including those that are NAT positive, have acceptable outcomes with similar early to midterm survival as recipients of HCV-negative organs.

Cardiac Amyloidosis: A Rare Cause of Recurrent Chylothorax.

Amyloidosis is caused by the extracellular deposition of fibrils composed of low molecular weight protein subunits. Its two main types are amyloid light chain (AL) amyloidosis and amyloid A (AA) amyloidosis (previously referred to as secondary amyloidosis). Clinical manifestations are dependent upon location, type, and amount of deposit. We report a case of a 72-year-old female who presented to the emergency department for evaluation of cough, fatigue, and shortness of breath. Physical examination was notable for decreased breath sounds bilaterally over the lower lung fields. Computed tomography (CT) of the chest showed a large lobulated right pleural effusion and atelectasis. Two liters of milky, white pleural fluid was removed via thoracocentesis, and pleural fluid analysis was consistent with chylothorax. Over the next 10-day period, there was a reaccumulation of the pleural fluid, which required a pleural catheter placement. The patient underwent video-assisted thoracoscopic surgery with pleural and pericardial tissue biopsy that was consistent with kappa or lambda AL amyloid. Unfortunately, her respiratory status subsequently declined, requiring mechanical ventilation, and eventually leading to cardiac arrest. Cardiac amyloidosis can rarely cause chylous ascites and chylothorax. The absence of electrocardiographic findings of left ventricular hypertrophy combined with apparent left ventricular hypertrophy on echocardiography is strongly suggestive of infiltrative cardiomyopathy such as cardiac amyloidosis. In these cases, cardiac amyloidosis should be considered in the differential diagnosis of chylothorax.

Development of a Dual Drug-Loaded, Surfactant-Stabilized Contrast Agent Containing Oxygen.

Co-delivery of cancer therapeutics improves efficacy and encourages synergy, but delivery faces challenges, including multidrug resistance and spatiotemporal distribution of therapeutics. To address these, we added paclitaxel to previously developed acoustically labile, oxygen-core, surfactant-stabilized microbubbles encapsulating lonidamine, with the aim of developing an agent containing both a therapeutic gas and two drugs acting in combination. Upon comparison of unloaded, single-loaded, and dual-loaded microbubbles, size (~1.7 µm) and yield (~2 × 109 microbubbles/mL) (~1.7) were not statistically different, nor were acoustic properties (maximum in vitro enhancements roughly 18 dB, in vitro enhancements roughly 18 dB). Both drugs encapsulated above required doses calculated for head and neck squamous cell carcinoma, the cancer of choice. Interestingly, paclitaxel encapsulation efficiency increased from 1.66% to 3.48% when lonidamine was included. During preparation, the combination of single drug-loaded micelles gave higher encapsulation (µg drug/g microbubbles) than micelles loaded with either drug alone (lonidamine, 104.85 ± 22.87 vs. 87.54 ± 16.41), paclitaxel (187.35 ± 8.38 vs. 136.51 ± 30.66). In vivo intravenous microbubbles produced prompt ultrasound enhancement within tumors lasting 3-5 min, indicating penetration into tumor vasculature. The ability to locally destroy the microbubble within the tumor vasculature was confirmed using a series of higher intensity ultrasound pulses. This ability to locally destroy microbubbles shows therapeutic promise that warrants further investigation.

Mechanistic insight into the adsorption of mercury (II) on the surface of red mud supported nanoscale zero-valent iron composite.

Recently, nanoscale zero-valent iron (nZVI) particles have been efficiently used in the remediation of many heavy metals, yet potential agglomeration and loss of nZVI remain a critical area of research. In this study, we used red mud as a stable supporting medium to develop red mud modified nZVI to form (RM-nZVI) composite. We assessed its sorptive/reductive removal of mercury (Hg2+) from aqueous solutions. The RM-nZVI was synthesized through the reduction of ferric iron by sodium borohydride (NaBH4) in the presence of red mud. Morphological characterization of RM-nZVI confirmed its diffusion state with lesser aggregation. The RM-nZVI has the BET surface area, pore diameter, and pore volume as 111.59 m2g-1, 3.82 nm, and 0.49 cm3g-1, respectively. Adsorption of mercury (Hg2+) by RM-nZVI exhibits pH-dependent behavior with increased removal of Hg2+ with the increase in pH up to 5, and the removal rate decreased gradually as the pH increased from 5 to 10. Extensive characterization of RM-nZVI corroborated the evidence that the removal of Hg2+ was initially by rapid physical adsorption, followed by a reduction of Hg2+ to Hg0. The adsorption data were best fitted with Langmuir isotherm with R2 (correlation coefficient) > 0.99 with high uptake capacity of 94.58 (mg g-1). The novel RM-nZVI composite with enhanced sorptive and reductive capacity is an ideal alternative for removing Hg2+ from contaminated water.

Case Report: Severe SARS-CoV-2 Infection Treated with Remdesivir in a Patient with ESRD.

BACKGROUND: The novel coronavirus disease 2019 (COVID-19) has led to a global pandemic since its emergence from Wuhan, China, in December of 2019. As research continues to evolve, there is a paucity of reports describing the management and treatment of COVID-19 in patients with acute kidney failure and End-Stage Renal Disease (ESRD). These patients have increased susceptibility to developing severe clinical symptoms from SARS-CoV-2 infection due to their underlying comorbidities. Remdesivir has emerged as a promising antiviral drug against SARS-CoV-2. However, data regarding the clinical benefits of remdesivir in patients with severe renal impairment is unavailable as they have been excluded from clinical trials due to the risk of sulfobutylether-ß-cyclodextrin (SBECD) accumulation in patients with eGFR<30 ml/min per 1.73m2. CASE PRESENTATION: We present the first case of a 47-year-old male with end-stage renal disease who was successfully treated with remdesivir during hospitalization for acute respiratory distress syndrome and respiratory failure arising from COVID-19. The worsening clinical progress of the patient despite intensive care and treatment with intravenous azithromycin therapy led to the decision to utilize remdesivir after a risk-benefit analysis, despite his eGFR being <15 ml/min per 1.73m2. Although the patient developed reversible hepatotoxicity, marked improvement of symptoms was observed after the five-day course of remdesivir was completed. CONCLUSION: Our findings describe the first instance of compassionate use of remdesivir for the treatment of COVID-19 in the setting of end-stage renal disease, acute respiratory distress syndrome, and hypoxemic respiratory failure.

HOPX Plays a Critical Role in Antiretroviral Drugs Induced Epigenetic Modification and Cardiac Hypertrophy.

People living with HIV (PLWH) have to take an antiretroviral therapy (ART) for life and show noncommunicable illnesses such as chronic inflammation, immune activation, and multiorgan dysregulation. Recent studies suggest that long-term use of ART induces comorbid conditions and is one of the leading causes of heart failure in PLWH. However, the molecular mechanism of antiretroviral drugs (ARVs) induced heart failure is unclear. To determine the mechanism of ARVs induced cardiac dysfunction, we performed global transcriptomic profiling of ARVs treated neonatal rat ventricular cardiomyocytes in culture. Differentially expressed genes were identified by RNA-sequencing. Our data show that ARVs treatment causes upregulation of several biological functions associated with cardiotoxicity, hypertrophy, and heart failure. Global gene expression data were validated in cardiac tissue isolated from HIV patients having a history of ART. Interestingly, we found that homeodomain-only protein homeobox (HOPX) expression was significantly increased in cardiomyocytes treated with ARVs and in the heart tissue of HIV patients. Furthermore, we found that HOPX plays a crucial role in ARVs mediated cellular hypertrophy. Mechanistically, we found that HOPX plays a critical role in epigenetic regulation, through deacetylation of histone, while the HDAC inhibitor, Trichostatin A, can restore the acetylation level of histone 3 in the presence of ARVs.

Mechanical activation of the angiotensin II type 1 receptor contributes to abdominal aortic aneurysm formation.

OBJECTIVE: The angiotensin II type 1 receptor (AT1R) can be activated under conditions of mechanical stretch in some cellular systems. Whether this activity influences signaling within the abdominal aorta to promote to abdominal aortic aneurysm (AAA) development remains unknown. We evaluated the hypothesis that mechanical AT1R activation can occur under conditions of hypertension (HTN) and contribute to AAA formation. METHODS: BPH/2 mice, which demonstrate spontaneous neurogenic, low-renin HTN, and normotensive BPN/3 mice underwent AAA induction via the calcium chloride model, with or without an osmotic minipump delivering 30 mg/kg/d of the AT1R blocker Losartan. Systolic blood pressure (SBP) was measured at baseline and weekly via a tail cuff. The aortic diameter (AoD) was measured at baseline and terminal surgery at 21 days by digital microscopy. Aortic tissue was harvested for immunoblotting (phosphorylated extracellular signal-regulated kinase-1 and -2 [pERK1/2] to ERK1/2 ratio) and expressed as the fold-change from the BPN/3 control mice. Aortic vascular smooth muscle cells (VSMCs) underwent stretch with or without Losartan (1 µM) treatment to assess the mechanical stimulation of ERK1/2 activity. Statistical analysis of the blood pressure, AoD, and VSMC ERK1/2 activity was performed using analysis of variance. However, the data distribution was determined to be log-normal (Shapiro-Wilk test) for ERK1/2 activity. Therefore, it was logarithmically transformed before analysis of variance. RESULTS: At baseline, the SBP was elevated in the BPH/2 mice relative to the BPN/3 mice (P < .05). Losartan treatment significantly reduced the SBP in both mouse strains (P < .05). AAA induction did not affect the SBP. At 21 days after induction, the percentage of increase in the AoD from baseline was significantly greater in the BPH/2 mice than in the BPN/3 mice (101.28% ± 4.19% vs 75.59% ± 1.67% above baseline; P < .05). Losartan treatment significantly attenuated AAA growth in both BPH/2 and BPN/3 mice (33.88% ± 2.97% and 43.96% ± 3.05% above baseline, respectively; P < .05). ERK1/2 activity was increased approximately fivefold in the BPH/2 control mice relative to the BPN/3 control mice (P < .05). In the BPH/2 and BPN/3 mice with AAA, ERK1/2 activity was significantly increased relative to the respective baseline control (P < .05) and effectively reduced by concomitant Losartan therapy (P < .05). Biaxial stretch of the VSMCs in the absence of angiotensin II demonstrated increased ERK1/2 activation (P < .05 vs static control), which was significantly inhibited by Losartan. CONCLUSIONS: In BPH/2 mice with spontaneous neurogenic, low-renin HTN, AAA growth was amplified compared with the normotensive control and was effectively attenuated using Losartan. ERK1/2 activity was significantly elevated in the BPH/2 mice and after AAA induction in the normotensive and hypertensive mice but was attenuated by Losartan treatment. These data suggest that AT1R activation contributes to AAA development. Therefore, further investigation into this signaling pathway could establish targets for pharmacotherapeutic engineering to slow AAA growth. (JVS-Vascular Science 2021;2:194-206.). CLINICAL RELEVANCE: Hypertension (HTN) and abdominal aortic aneurysm (AAA) have been epidemiologically linked for decades; however, a biomechanical link has not yet been identified. Using a murine model of spontaneous neurogenic HTN experimentally demonstrated to have low circulating renin, mechanical activation of the angiotensin II type 1 receptor (AT1R) was identified with elevated blood pressure and AAA induction. HTN amplified AAA growth. However, more importantly, blocking the activation of AT1R with the angiotensin receptor blocker Losartan effectively abrogated AAA development. Although inhibiting the production of angiotensin II has previously been unsuccessful in altering AAA growth, the results from the present study suggest that blocking the activation of AT1R through direct ligand binding or mechanical stimulation might alter aortic wall signaling and warrants further investigation.

A Case Series of Elizabethkingia meningosepticum Bacteremia in the Cancer Population.

Elizabethkingia meningosepticum (E. meningosepticum) is a ubiquitous microorganism previously known as Chryseobacterium meningosepticum. It is emerging as a pathogen responsible for bacteremia in the immunocompromised population, particularly in cancer patients and those with a history of prolonged hospital stay and frequent instrumentations. A retrospective chart review of all cases over 10 years at the Moffitt Cancer Center showed a total of three patients with E. meningosepticum infection. The first patient (history of multiple myeloma) underwent endoscopy complicated by aspiration pneumonia and positive blood culture for E. meningosepticum infection. The second patient (current acute myelogenous leukemia) had neutropenic fever in the setting of a recent chest port infection. Blood culture from the chest port showed E. meningosepticum. The third patient (history of esophageal adenocarcinoma and acute myelogenous leukemia) had a history of recent pneumonia and cellulitis who presented with recurrent neutropenic fever. Blood culture was positive for E. meningosepticum. E. meningosepticum bacteremia has a high 28-day mortality rate (41%). As these three cases illustrate, early identification of the pathogen along with empiric treatment with a fluoroquinolone and/or minocycline is indicated to reduce morbidity and mortality.

COVID-19 in Immunocompromised Cancer Patients: A Case Series and Review of the Literature.

The global pandemic of the novel coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has presented newfound challenges to the oncology community regarding management of disease progression in immunocompromised and cancer patients. Further, the large influx of COVID-19 patients has overwhelmed healthcare facilities, limited access to intensive care unit beds and ventilators, and canceled elective surgeries causing disruptions to the cancer care continuum and re-organization of oncological care. While it is known that the potential threat of infection is greatest in elderly patients (>60 years of age) and patients with underlying comorbidities, there is still insufficient data to determine the risk of COVID-19 in cancer patients. Given the immunosuppressive status in cancer patients arising from chemotherapy and other comorbidities, management of COVID-19 in this patient population carries a unique set of challenges. We report three cases of COVID-19 in immunocompromised cancer patients and discuss the challenges in preventing, diagnosing, and treating this vulnerable group.