Continuing Medical Education onlineThis activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Medscape, LLC and the American Society of Hematology. Medscape, LLC is accredited by the ACCME to provide continuing medical education for physicians. Medscape, LLC designates this Journal-based CME activity for a maximum of 1.0 AMA PRA Category 1 Credit(s) ™ . Physicians should claim only the credit commensurate with the extent of their participation in the activity. All other clinicians completing this activity will be issued a certificate of participation. To participate in this journal CME activity: (1) review the learning objectives and author disclosures; (2) study the education content; (3) take the post-test with a 70% minimum passing score and complete the evaluation at http://www.medscape.org/journal/blood; and (4) view/print certificate. For CME questions, see page 2969. Disclosures The authors, the Associate Editor Martin S. Tallman, and CME questions author Laurie Barclay, freelance writer and reviewer, Medscape, LLC, declare no competing financial interests. Learning objectives Upon completion of this activity, participants will be able to:1. Describe the prevalence and clinical characteristics of parainfluenza virus (PIV) infections in patients with leukemia or HSCT, based on a medical record review.2. Describe outcomes of PIV infections in patients with leukemia or HSCT and the factors predicting progression to pneumonia, based on a medical record review.3. Describe risk factors for mortality from PIV infections in patients with leukemia or HSCT, based on a medical record review.

ABSTRACTEscherichia colisequence type ST131 (from phylogenetic group B2), often carrying the extended-spectrum-β-lactamase (ESBL) geneblaCTX-M-15, is an emerging globally disseminated pathogen that has received comparatively little attention in the United States. Accordingly, a convenience sample of 351 ESBL-producingE. coliisolates from 15 U.S. centers (collected in 2000 to 2009) underwent PCR-based phylotyping and detection of ST131 andblaCTX-M-15. A total of 200 isolates, comprising 4 groups of 50 isolates each that were (i)blaCTX-M-15negative non-ST131, (ii)blaCTX-M-15positive non-ST131, (iii)blaCTX-M-15negative ST131, or (iv)blaCTX-M-15positive ST131, also underwent virulence genotyping, antimicrobial susceptibility testing, and pulsed-field gel electrophoresis (PFGE). Overall, 201 (57%) isolates exhibitedblaCTX-M-15, whereas 165 (47%) were ST131. ST131 accounted for 56% ofblaCTX-M-15-positive- versus 35% ofblaCTX-M-15-negative isolates (P< 0.001). Whereas ST131 accounted for 94% of the 175 total group B2 isolates, non-ST131 isolates were phylogenetically distributed byblaCTX-M-15status, with groups A (blaCTX-M-15-positive isolates) and D (blaCTX-M-15-negative isolates) predominating. BothblaCTX-M-15and ST131 occurred at all participating centers, were recovered from children and adults, increased significantly in prevalence post-2003, and were associated with molecularly inferred virulence. Compared with non-ST131 isolates, ST131 isolates had higher virulence scores, distinctive virulence profiles, and more-homogeneous PFGE profiles.blaCTX-M-15was associated with extensive antimicrobial resistance and ST131 with fluoroquinolone resistance. Thus,E. coliST131 andblaCTX-M-15are emergent, widely distributed, and predominant among ESBL-positiveE. colistrains in the United States, among children and adults alike. Enhanced virulence and antimicrobial resistance have likely promoted the epidemiological success of these emerging public health threats.

us-map.html ¶ A list of severe manifestations of monkeypox can be found at https://emergency. cdc.gov/han/2022/han00475.asp. ** During the study period and as of October 21, 2022, CDC was notified by state and local jurisdictions of five decedents whose death certificates included monkeypox as a cause of death or contributing factor, six decedents whose cause of death is still under active investigation, and one decedent in whom the death was not monkeypox-related. Additional monkeypox cases involving severe disease or death might not be included in this report if CDC has not yet been notified about the case or if the case occurred outside of the study period.

BACKGROUND: Pandemic influenza A (hereafter 2009/H1N1) caused significant morbidity and mortality during the 2009 pandemia. Patients with chronic medical conditions and immunosuppressive diseases had a greater risk of complications. However, data regarding the characteristics and outcome of 2009/H1N1 infection in patients with solid tumors are nonexistent. Herein, the authors describe a series of influenza 2009/H1N1 in patients with solid malignancies at 3 major cancer hospitals worldwide. METHODS: The authors retrospectively reviewed the records of patients with solid organ malignancies and 2009/H1N1 from The University of Texas M. D. Anderson Cancer Center in Houston, Texas; the Mexican National Cancer Institute, Federal District of Mexico; and King Hussein Cancer Center in Amman, Jordan from the period of the 2009 H1N1 pandemia. Data on demographics, disease characteristics, and outcome were extracted. RESULTS: In total, 115 cases were identified during the pandemic influenza among the 3 institutions. High rates of hospitalization (50%), pneumonia (23%), and death (9.5%) were reported. Patients who developed pneumonia and those who died were moderately to severely immunocompromised (P = .001 and P = .006, respectively). A multivariate competing risk analysis demonstrated that a delay >48 hours in starting antiviral therapy was associated significantly with an increased risk of developing pneumonia (P = .013). CONCLUSIONS: The 2009/H1N1 pandemic caused severe illness in immunocompromised patients with cancer who had solid tumors, and heavily immunosuppressed patients were at greater risk of developing pneumonia and death. Early initiation of antiviral therapy is crucial in this patient population to decrease morbidity and probably mortality. Cancer 2012. © 2012 American Cancer Society.

E. coli pyomyositis has emerged as a serious problem among our patients with hematologic malignancy. It usually is caused by members of E. coli ST131, a recently identified cause of fluoroquinolone-resistant, ESBL-positive E. coli infection worldwide. Awareness of this emerging syndrome and the usual causative agent is important to ensure appropriate management when febrile, neutropenic patients with hematologic malignancy exhibit signs of localized muscle infection.

Viral infections have always been considered pediatric diseases. However, viral pneumonia has become an important cause of morbidity and mortality in immuncompromised adults. Improved diagnostic techniques, such as the introduction of highly sensitive nucleic acid amplification tests, have not only allowed us to discover new viruses but also to determine the etiology of viral pneumonia in immunocompromised adult hosts. Unfortunately, only a few antiviral agents are available. Thus, early diagnosis and treatment are crucial to patient outcome. In this article, we review the most common viruses that have been implicated as etiologic agents of viral pneumonia in immunocompromised adults. We discuss the epidemiologic characteristics and clinical presentation of these viral infections and the most appropriate diagnostic approaches and therapies when available.

Here, we report a case of a 60-year-old renal transplant recipient who developed an intra-abdominal abscess which grew a carbapenem-resistant Lactobacillus casei. This is significant since it is the first report of a clinical isolate of Lactobacillus sp. that demonstrated both microbiological and clinical resistance to carbapenem use. Moreover, the probiotic supplement that the patient had taken also grew a similar organism raising the concern of probiotic associated infection in immunocompromised individual.

Background New therapies to achieve hepatitis B surface antigen (HBsAg) clearance are under development. However, gaps in knowledge exist in understanding the incidence and predictors of HBsAg clearance in a racially diverse HIV population. Methods We examined the incidence and risk of HBsAg clearance in a retrospective cohort of people living with HIV/HBV. Included patients had sufficient data to establish chronic infection based on CDC guidelines. We examined the incident rate for HBsAg loss and hazard rate ratios to evaluate predictors for HBsAg clearance in a multivariable model. Results Among the 571 HIV/HBV, 87% were male, 61% Black, 45% had AIDS, 48% HBeAg-positive, and median follow-up was 88 months. Incident HBsAg clearance was 1.5 per 100 person-years. In multivariate model, AIDS at baseline [adjusted hazard ratio [(aHR) 2.43, 95% CI:1.37,4.32 ], Hispanics (aHR 3.57, 95% CI: 1.33, 9.58), and those with injection drug use as an HIV risk factor (aHR, 3.35, 95% CI: 1.26, 8.89) were more likely to lose HBsAg whereas those who were HBeAg-positive (aHR 0.34, 0.19, 0.63) were less likely to lose HBsAg. Median change in CD4 cell count during the observation period was 231 cells/mm 3 in those with HBsAg loss vs. 112 cells/mm 3 in those with HBsAg persistence (p=0.004). Conclusion HBsAg loss occurs in about 10% of those with chronic HBV-infection. Hispanics, AIDS at baseline, injection drug use history, and HBeAg-negative status at baseline predicted the likelihood of HBsAg loss. Immune restoration may be a mechanism through which HBsAg loss occurs in HIV patients.