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The authors comments on the extraordinary alert issued by the U.S. Centers for Disease Control and Prevention (CDC) on June 24, 2016 which advise the healthcare facilities in all state regarding the Candida auris in patients. They mentions the recovered C. auris from healthcare facilities announced by the Public Health England (PHE).

The article describes the case of a 62-year-old man with ischemic cardiomyopathy who underwent orthotopic heart transplantation and was diagnosed with disseminated toxoplasmosis with pneumonia and septic shock. It was found that the organ donor was immunoglobulin G (IgG) seropositive for the protozoan parasite Toxoplasma gondii and that the patient was not receiving prophylactic therapy as an inpatient. The patient succumbed to infection and an autopsy showed disseminated Toxoplasma tachyzoites and bradyzoites.

Candida albicans in the immunocompetent host is a benign member of the human microbiota. Though, when host physiology is disrupted, this commensal-host interaction can degenerate and lead to an opportunistic infection. Relatively little is known regarding the dynamics of C. albicans colonization and pathogenesis. We developed a C. albicans cell surface protein microarray to profile the immunoglobulin G response during commensal colonization and candidemia. The antibody response from the sera of patients with candidemia and our negative control groups indicate that the immunocompetent host exists in permanent host-pathogen interplay with commensal C. albicans. This report also identifies cell surface antigens that are specific to different phases (i.e. acute, early and mid convalescence) of candidemia. We identified a set of thirteen cell surface antigens capable of distinguishing acute candidemia from healthy individuals and uninfected hospital patients with commensal colonization. Interestingly, a large proportion of these cell surface antigens are involved in either oxidative stress or drug resistance. In addition, we identified 33 antigenic proteins that are enriched in convalescent sera of the candidemia patients. Intriguingly, we found within this subset an increase in antigens associated with heme-associated iron acquisition. These findings have important implications for the mechanisms of C. albicans colonization as well as the development of systemic infection. [ABSTRACT FROM AUTHOR]

The article analyzes the correlation of the virulence of 18 Cryptococcus neoformans var. grubii isolates from AIDS patients with expression of several well-described virulence factors. The study highlights that a large part of an organism's disease causing potential in humans is shaped by the person's immune status and other host factors such as genetic characteristics.

Candida is the third most common cause of bloodstream infections in hospitalized patients. Immunity to C. albicans, the most frequent species to be isolated in candidiasis, involves a well-characterized Dectin-l/caspase-associated recruitment domain adaptor 9 (CARD91/TL-I7 signaling axis. Infections caused by non-albicans Candida species are on the rise, but surprisingly little is known about immunity to these pathogens. In this study, we evaluated a systemic infection model of C. tropicalis, a clinically relevant, but poorly understood, non -albicans Candida. Mice lacking CARD9 were profoundly susceptible to C. tropicalis, displaying elevated fungal burdens in visceral organs and increased mortality compared with wild-type (WT) controls. Unlike C. albicans, IL-17 responses were induced normally in CARD9-/- mice following C. tropicalis infection. Moreover, there was no difference in susceptibility to C. tropicalis infection between WTand IL-23pl9-/-, IL-17RA-/-, or Actl-/- mice. However, TNF-α expression was markedly impaired in CARI)9-/- mice. Consistently, WT mice depleted of TNF-α were more susceptible to C. tropicalis, and CARD9-deficient neutrophils and monocytes failed to produce TNF-α following stimulation with C. tropicalis Ags. Both neutrophils and monocytes were necessary for defense against C. tropicalis, because their depletion in WT mice enhanced susceptibility to C. tropicalis. Disease in CARD9-/- mice was not due to defective neutrophil or monocyte recruitment to infected kidneys. However, TNF-α treatment of neutrophils in vitro enhanced their ability to kill C. tropicalis. Thus, protection against systemic C. tropicalis infection requires CARD9 and TNF-α, but not IL-17, signaling. Moreover, CARD9-dependent production of TNF-α enhances the candidacidal capacity of neutrophils, limiting fungal disease during disseminated C. tropicalis infection. [ABSTRACT FROM AUTHOR]

Background: Multidrug-resistant Enterobacterales (MDR-E), including carbapenem-resistant and third-generation cephalosporin-resistant Enterobacterales (CRE, CefR-E), are major pathogens following solid organ transplantation (SOT)., Methods: We prospectively studied patients who underwent lung, liver, and small bowel transplant from February 2015 through March 2017. Weekly perirectal swabs (up to 100 days post-transplant) were cultured for MDR-E. Whole-genome sequencing (WGS) was performed on gastrointestinal (GI) tract-colonizing and disease-causing isolates., Results: Twenty-five percent (40 of 162) of patients were MDR-E GI-colonized. Klebsiella pneumoniae was the most common CRE and CefR-E. Klebsiella pneumoniae carbapenemases and CTX-M were leading causes of CR and CefR, respectively. Thirty-five percent of GI colonizers developed MDR-E infection vs 2% of noncolonizers (P < .0001). The attack rate was higher among CRE colonizers than CefR-E colonizers (53% vs 21%, P = .049). GI colonization and high body mass index were independent risk factors for MDR-E infection (P ≤ .004). Thirty-day mortality among infected patients was 6%. However, 44% of survivors developed recurrent infections; 43% of recurrences were late (285 days to 3.9 years after the initial infection). Long-term survival (median, 4.3 years post-transplant) did not differ significantly between MDR-E-infected and MDR-E-noninfected patients (71% vs 77%, P = .56). WGS phylogenetic analyses revealed that infections were caused by GI-colonizing strains and suggested unrecognized transmission of novel clonal group-258 sublineage CR-K. pneumoniae and horizontal transfer of resistance genes., Conclusions: MDR-E GI colonization was common following SOT and predisposed patients to infections by colonizing strains. MDR-E infections were associated with low short- and long-term mortality, but recurrences were frequent and often occurred years after initial infections. Findings provide support for MDR-E surveillance in our SOT program., (© The Author(s) 2021. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.)

Infection of subcutaneous tissue by black fungi (subcutaneous phaeohyphomycosis) has only been reported in six transplant patients, all of whom were solid organ recipients. These patients presented with indolent, localized infections at least 1 year after transplant, while on maintenance immunosuppressive regimens. They were cured by surgical resection, either alone or in conjunction with antifungal agents. We report a case of subcutaneous phaeohyphomycosis occurring in a bone marrow transplant recipient receiving high doses of immunosuppressive agents, in whom widespread subcutaneous infection due to Exophiala jeanselmei was not eradicated by repeated resections and therapy with amphotericin B and flucytosine. The infection was eventually cured after addition of itraconazole to the therapeutic regimen. Results of in vitro testing of the isolate for susceptibility to a combination of amphotericin B, flucytosine and itraconazole confirmed the potential role of combination antifungal therapy in the setting of refractory infection.