Search

Disseminated histoplasmosis (DH) often mimics other diseases, leading to misdiagnosis and delays in treatment. We present a patient who developed DH after treatment with immunosuppressants for an initial diagnosis of inflammatory bowel disease (IBD). Upon diagnosing her with DH, liposomal amphotericin B was started, and she eventually recovered after a prolonged hospitalization. Intrabdominal histoplasmosis has many similarities with IBD. Treatment with immunosuppressants in undiagnosed histoplasmosis can lead to dissemination with potentially catastrophic results.

Empyema necessitans is a relatively rare clinical entity in which the empyema extends through the parietal pleura into the adjacent soft tissue and musculature of the chest wall. It usually occurs due to inadequate treatment of a primary lung infection. Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans is a facultative anaerobic gram-negative coccobacillus that is part of the normal oral flora. Infections due to this organism usually result from aspiration in conjunction with dental disease or trauma to the oral mucosa resulting in pneumonia or empyema. It often coinfects with Actinomyces and is known to cause empyema necessitans. Cases of monomicrobial empyema necessitans due to Aggregatibacter actinomycetemcomitans in adults have rarely been reported with four such publications found on review of the literature. We present a patient with severe periodontitis who developed empyema necessitans due to Aggregatibacter actinomycetemcomitans likely from aspiration complicated by pyomyositis of the right triceps brachii and a left posterior thigh abscess.

Background Early in the COVID-19 pandemic, tenofovir (TAF/TDF) was identified as a potential agent for SARS-CoV-2 due to binding to RNA-dependent RNA polymerase similarly to remdesivir. This led to the hypothesis that TAF/TDF may be lessening the severity and improving outcomes of COVID-19 infection. COVID-19 Severity COVID-19 Infection Outcomes Methods Patients were identified by searching for HIV infection and SARS-CoV2 PCR testing. Type of antiretroviral therapy (ART), CD4+ cell count, HIV viral load (VL), comorbidities, presenting symptoms, severity of COVID infection, and outcomes were analyzed. COVID disease was classified as mild, moderate, severe, or critical based on World Health Organization criteria. We primarily sought to determine the effect of TAF/TDF on the severity of COVID infection. The secondary endpoint was to determine the effect of low CD4 count and HIV VL on the severity of infection. Results 39 HIV+ patients were tested at least once for SARS-CoV2 by PCR at VA NJ Health Care System. 18 of 39 patients were PCR positive. In those, common presenting symptoms included: fever (15/18), cough (7/18), and lethargy/fatigue (6/18). 16 of the 39 HIV+ patients’ ART included TAF/TDF; 8 of 18 COVID+ and 8 of 21 COVID-. In the COVID- group, 2 patients had CD4 count < 200 cells/mm3, 3 patients had HIV VL >200, and 19 of 21 had at least 1 comorbidity. In the COVID+ group, 3 had CD4 count < 200 cells/mm3, none had detectible HIV viremia, and all but one had comorbidities. Of COVID+ infections, 7 were mild, 3 moderate, 8 severe, and 5 patients died. 4 of the 5 patients that did not survive were in non-TAF/TDF group. All 3 patients with CD4 count < 200 cells/mm3 had severe disease. 6 out of 8 patients developed mild disease in TAF/TDF group vs. 1 out of 10 patients in non-TAF/TDF group. 1 out of 8 and 7 out of 10 patients had severe or critical disease in TAF/TDF vs non-TAF/TDF groups respectively. Conclusion In this sample of 18 HIV+ patients with COVID-19 infection, patients receiving TAF/TDF were more likely to develop mild disease and have full recovery than those who were on TAF/TDF-free regimens (75% vs. 10% and 87.5% vs. 50%, respectively). Patients not on TAF/TDF-based regimens had a higher rate of developing severe and critical COVID-19 disease (40% vs. 0% and 30% vs. 12.5%, respectively). Disclosures All Authors: No reported disclosures

Breast cancer stem cells (BCSCs) constitute a subpopulation of tumor cells that express stem cell-associated markers and have a high capacity for tumor generation in vivo. Identification of BCSCs from tumor samples or breast cancer cell lines has been based mainly on CD44(+)/CD24(-/low) or ALDH(+) phenotypes. BCSCs isolation has allowed the analysis of the molecular mechanisms involved in their origin, self-renewal, differentiation into tumor cells, resistance to radiation therapy and chemotherapy, and invasiveness and metastatic ability. Molecular genetic analysis using knockout animals and inducible transgenics has identified NF-κB, c-Jun, p21(CIP1), and Forkhead-like-protein Dach1 involvement in BCSC expansion and fate. Clinical analyses of BCSCs in breast tumors have found a correlation between the proportion of BCSCs and poor prognosis. Therefore, new therapies that specifically target BCSCs are an urgent need. We summarize recent evidence that partially explain the biological characteristics of BCSCs.

Cyclin D1 overexpression is found in more than 50% of human breast cancers and causes mammary cancer in transgenic mice. Dysregulation of cyclin D1 gene expression or function contributes to the loss of normal cell cycle control during tumorigenesis. Recent studies have demonstrated that cyclin D1 conducts additional specific functions to regulate gene expression in the context of local chromatin, promote cellular migration and inhibit mitochondrial metabolism. It is anticipated that these additional functions contribute to the pathology associated with dysregulated cyclin D1 abundance. This article discusses evidence that examines the significance of cyclin D1 in breast cancer with emphasis on its role in breast cancer stem cell expansion.