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Woman at a lectern

Woman at a lectern

Exciting session at #fungal26 in Asilomar on Emerging and are-emerging Fungal Pathogens

First talk is from award winning scientist, @ameliabarberphd.bsky.social on Candida parapsilosis #MedMycoSky

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Two men in front of sunset on the beach

Two men in front of sunset on the beach

Four people smiling

Four people smiling

Asilomar #fungal26
Who will win the coveted Schwartzy award this year? 🏆 #MedMycoSky

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VVC State-of-the-Art visual abstract

VVC State-of-the-Art visual abstract

State-of-the-Art Review: Managing Vulvovaginal Candidiasis

Riina Rautemaa-Richardson, Jack Sobel, @drneilstone.bsky.social Francesco de Seta, et al, and Elena Roselletti

doi.org/10.1093/cid/...

#IDSky #MedMycoSky #GynSky @cidjournal.bsky.social

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Fig 1 Mechanism of action of different classes of antifungals. AmB is Amphotericin B; cAmB is the encochleated form of Amphotericin B; L-AmB is liposomal Amphotericin B.

Fig 1 Mechanism of action of different classes of antifungals. AmB is Amphotericin B; cAmB is the encochleated form of Amphotericin B; L-AmB is liposomal Amphotericin B.

Fig 2 Pharmacokinetic profile of liposomal amphotericin B

Fig 2 Pharmacokinetic profile of liposomal amphotericin B

Fig 3 Amphotericin B (AmB) activity and fungal resistance mechanisms. The upper panel shows AmB’s dual action:pore formation via ergosterol binding and oligomerization, and the “sterol sponge” mechanism, which sequesters ergosterol from membranes. Mitochondria-associated oxidative stress also contributes to fungal killing. The lower panel summarizes key resistance strategies: (i) ergosterol pathway alterations, generating sterols with reduced AmB affinity; (ii) enhanced oxidative stress defenses, including increased catalase activity with a consequent reduction in oxidative stress response; and (iii) biofilm formation, limiting drug penetration

Fig 3 Amphotericin B (AmB) activity and fungal resistance mechanisms. The upper panel shows AmB’s dual action:pore formation via ergosterol binding and oligomerization, and the “sterol sponge” mechanism, which sequesters ergosterol from membranes. Mitochondria-associated oxidative stress also contributes to fungal killing. The lower panel summarizes key resistance strategies: (i) ergosterol pathway alterations, generating sterols with reduced AmB affinity; (ii) enhanced oxidative stress defenses, including increased catalase activity with a consequent reduction in oxidative stress response; and (iii) biofilm formation, limiting drug penetration

Fig 4 Recommendations for L-AmB therapy in resistant and refractory fungal infections.

Fig 4 Recommendations for L-AmB therapy in resistant and refractory fungal infections.

Current opinion on the potential role of liposomal amphotericin B in underexplored clinical scenarios

Angelino and colleagues in CMR

*supported by unrestricted grant from Gilead, who make Ambisome®️

journals.asm.org/doi/10.1128/... #MedMycoSky #IDSky

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Preview
Antibiotic-induced microbiota disruption impairs neutrophil-mediated immunity to respiratory Aspergillus fumigatus infection in mice | mBio Aspergillus fumigatus is an environmental mold that causes invasive pulmonary disease in immunocompromised individuals. Owing to limited diagnostic tools, a narrow arsenal of effective treatments, and...

Might antibiotics increase risks of aspergillosis?

Antibiotic-induced microbiota disruption impairs neutrophil-mediated immunity to respiratory Aspergillus fumigatus infection in mice

Mariano A. Aufiero & @fungalspore.bsky.social

mBio journals.asm.org/doi/10.1128/... #IDSky #MedMycoSky

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Antifungal susceptibility testing across fungi: why MICs vary, methods diverge, and what MIC can miss Antifungal susceptibility testing (AFST) is central to antifungal stewardship; however, MIC results can be variable and may require careful interpretation because endpoints can be ambiguous, clinical ...

Antifungal susceptibility testing across fungi: why MICs vary, methods diverge, and what MIC can miss

Cornelia Lass-Flörl and colleagues

Open access in @cmijournal.bsky.social

www.clinicalmicrobiologyandinfection.org/article/S119... #IDSky #MedMycoSky

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Pathogen Factors Promoting Fungal Infection
Infectious Dose
- High initial inoculum exceeds immune clearance
Immune Evasion
Eg:
• B-glucan masking (C albicans, Histoplasma capsulatum)
• Capsule formation
(Cryptococcus neoformans)
• Melanin production (dematiaceous fungi)
• Biofilm production (Candida spp., A fumigatus)
Tissue Tropism
Examples:
• Aspergillus fumigatus for lung parenchyma
• C neoformans/
C. gattii for CNS tissues (meninges)
• Basidiobolus ranarum for bowel wall
• Trichophyton spp. strict tropism for keratinized tissues
• Aspergillus and Candida spp. for external auditory canal
Host Factors
Enabling Fungal Persistence
Immunosuppression or Innate Immune
Deficits Examples:
• CARD9 deficiency
• Diabetes mellitus
• Idiopathic CD4 lymphocytopenia
• Hematologic malignancies
• HIV/AIDS
Conditions and Comorbidities (Non-immunosuppressive)
Examples:
• Chronic lung diseases (e.g. prior pulmonary TB, COPD))
• Eczema/atopic dermatitis
• Heightened estrogen
• IVDU
• Previous surgeries
• Smoking
• Wounds or burns
Clinical Factors
Delaying Disease Resolution
Antibiotic and/or Steroid Use/Misuse
Eg:
• Bacterial pneumonia abx for coccidioidomycosis or histoplasmosis
• Topical steroid misuse for ringworm
Delayed Diagnosis or Misdiagnosis
Delayed diagnosis due to:
• Non-specific or overlapping clinical presentation
• Empiric treatment
• Limited access to diagnostics
• Long test turnaround times
• Lack of provider awareness
Misdiagnosis
Immunosuppressive Regimens 
Eg:
• Chemotherapy
• Organ transplantation
Steroids
Chronic Disease States
Affecting Body Systems
Respiratory
• Chronic pulmonary aspergillosis
• Chronic pulmonary coccidioidomycosis
• Chronic cavitary pulmonary histoplasmosis
Neurologic
• Cryptococcal meningoencephalitis
• Phaeohyphomycosis
• Coccidioidal meningitis
Cardiac
• endocarditis
GI
•  histoplasmosis
•  basidiobolomycosis
Sensory
•  keratitis
•  otitis
Mucosa, Skin & Bone
• T indotineae
• Recurrent vvc 
• Chromoblastomycosis
• Eumycetoma

Pathogen Factors Promoting Fungal Infection Infectious Dose - High initial inoculum exceeds immune clearance Immune Evasion Eg: • B-glucan masking (C albicans, Histoplasma capsulatum) • Capsule formation (Cryptococcus neoformans) • Melanin production (dematiaceous fungi) • Biofilm production (Candida spp., A fumigatus) Tissue Tropism Examples: • Aspergillus fumigatus for lung parenchyma • C neoformans/ C. gattii for CNS tissues (meninges) • Basidiobolus ranarum for bowel wall • Trichophyton spp. strict tropism for keratinized tissues • Aspergillus and Candida spp. for external auditory canal Host Factors Enabling Fungal Persistence Immunosuppression or Innate Immune Deficits Examples: • CARD9 deficiency • Diabetes mellitus • Idiopathic CD4 lymphocytopenia • Hematologic malignancies • HIV/AIDS Conditions and Comorbidities (Non-immunosuppressive) Examples: • Chronic lung diseases (e.g. prior pulmonary TB, COPD)) • Eczema/atopic dermatitis • Heightened estrogen • IVDU • Previous surgeries • Smoking • Wounds or burns Clinical Factors Delaying Disease Resolution Antibiotic and/or Steroid Use/Misuse Eg: • Bacterial pneumonia abx for coccidioidomycosis or histoplasmosis • Topical steroid misuse for ringworm Delayed Diagnosis or Misdiagnosis Delayed diagnosis due to: • Non-specific or overlapping clinical presentation • Empiric treatment • Limited access to diagnostics • Long test turnaround times • Lack of provider awareness Misdiagnosis Immunosuppressive Regimens Eg: • Chemotherapy • Organ transplantation Steroids Chronic Disease States Affecting Body Systems Respiratory • Chronic pulmonary aspergillosis • Chronic pulmonary coccidioidomycosis • Chronic cavitary pulmonary histoplasmosis Neurologic • Cryptococcal meningoencephalitis • Phaeohyphomycosis • Coccidioidal meningitis Cardiac • endocarditis GI • histoplasmosis • basidiobolomycosis Sensory • keratitis • otitis Mucosa, Skin & Bone • T indotineae • Recurrent vvc • Chromoblastomycosis • Eumycetoma

Contribution of fungal diseases to the U.S. chronic disease burden

From the CDC Mycotic Diseases Branch

journals.asm.org/doi/10.1128/... #IDSky #MedMycoSky

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Emerging risk factors for IFI in HCT. Climate change, older/comorbid recipients, antifungal prophylaxis, changes in GVHD prophylaxis and treatment, longer survivorship, agricultural use of antifungals

Emerging risk factors for IFI in HCT. Climate change, older/comorbid recipients, antifungal prophylaxis, changes in GVHD prophylaxis and treatment, longer survivorship, agricultural use of antifungals

Invasive Fungal Disease in Allogeneic Hematopoietic Cell Transplantation: New Risk Factors and New Therapeutic Options in a Changing World

@abbydouglas.bsky.social & Monica Slavin

doi.org/10.1111/tid.... #TxID #IDSky #MedMycoSky

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Graphical abstract showing summaries of the demographic data (M 71%, HIV 57%, SOT 18%, autoimmune disease 16%), sites of infection (CNS 91%, fungemia 60%, lung 40%), ICU management (mech ventilation 55%, pressers 34%, RRT 18%), and outcome (ICU mortality 42%, 90d mortality 50%)

Graphical abstract showing summaries of the demographic data (M 71%, HIV 57%, SOT 18%, autoimmune disease 16%), sites of infection (CNS 91%, fungemia 60%, lung 40%), ICU management (mech ventilation 55%, pressers 34%, RRT 18%), and outcome (ICU mortality 42%, 90d mortality 50%)

Presentation and prognosis of cryptococcosis requiring intensive care unit admission in France: the CRYPTO-ICU study

Retrospective study of 151 patients admitted to 30 French ICUs with cryptococcosis over 23 years

academic.oup.com/cid/advance-... #IDSky #TxID #CritCare #MedMycoSky

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Pathogenesis of Mucormycosis, Host Defenses, and Potential Future Therapeutic Targets.
Mucorales sporangiospores released into the air from sporangia are inhaled, and the sporangiospore coat protein CotH3 binds to GRP78 on the pseudostratified columnar epithelial cells of the upper resp tract, where the sporangiospores may germinate into hyphae to invade nasal airways and sinuses (Panel A). Sporangiospores, by means of another coat adhesin (CotH7), also bind to epidermal growth factor receptor (EGFR) and integrin α3β1 receptor on pulmonary alveolar epithelial cells of the lower respiratory tract, which triggers a downstream transcriptional response involving cytokines (interleukin-6 and interleukin-8), chemokines (CCL2 and CCL5), and intercellular adhesion molecule 1 (ICAM-1). Hyphal invasion also triggers production of hypoxia-inducible factor 1α (HIF1α) and release of proinflammatory cytokines. In wound-related mucormycosis, traumatic inoculation of fungal elements (found on the surfaces of rocks, wood, glass, and metal) into damaged tissue allows for the development of infection in a host with immune paralysis due to trauma. The release of endogenous host-derived molecules known as damage-associated molecular patterns (DAMPs) reduces phagocytosis, impairs chemotaxis, and induces immune paralysis. Mucoricin released by the invading hyphae induces death of immune and endothelial cells, which results in tissue necrosis and accelerates endovascular thrombosis, ischemia, and infarction (Panel B). PMNs and monocytes recognize early germinated sporangiospores by pattern recognition receptors (e.g., TLR2) that detect mucorales-associated molecular patterns (e.g., 1,3-βD-glucans exposed on hyphal structures). Intrinsic host colony-stimulating factors such as granulocyte–macrophage colony-stimulating factor (GM-CSF) and IFN-γ further contribute to augmentation of innate host defenses against the invading hyphae, which in turn dampen immune responses. Factors in the tissue …

Pathogenesis of Mucormycosis, Host Defenses, and Potential Future Therapeutic Targets. Mucorales sporangiospores released into the air from sporangia are inhaled, and the sporangiospore coat protein CotH3 binds to GRP78 on the pseudostratified columnar epithelial cells of the upper resp tract, where the sporangiospores may germinate into hyphae to invade nasal airways and sinuses (Panel A). Sporangiospores, by means of another coat adhesin (CotH7), also bind to epidermal growth factor receptor (EGFR) and integrin α3β1 receptor on pulmonary alveolar epithelial cells of the lower respiratory tract, which triggers a downstream transcriptional response involving cytokines (interleukin-6 and interleukin-8), chemokines (CCL2 and CCL5), and intercellular adhesion molecule 1 (ICAM-1). Hyphal invasion also triggers production of hypoxia-inducible factor 1α (HIF1α) and release of proinflammatory cytokines. In wound-related mucormycosis, traumatic inoculation of fungal elements (found on the surfaces of rocks, wood, glass, and metal) into damaged tissue allows for the development of infection in a host with immune paralysis due to trauma. The release of endogenous host-derived molecules known as damage-associated molecular patterns (DAMPs) reduces phagocytosis, impairs chemotaxis, and induces immune paralysis. Mucoricin released by the invading hyphae induces death of immune and endothelial cells, which results in tissue necrosis and accelerates endovascular thrombosis, ischemia, and infarction (Panel B). PMNs and monocytes recognize early germinated sporangiospores by pattern recognition receptors (e.g., TLR2) that detect mucorales-associated molecular patterns (e.g., 1,3-βD-glucans exposed on hyphal structures). Intrinsic host colony-stimulating factors such as granulocyte–macrophage colony-stimulating factor (GM-CSF) and IFN-γ further contribute to augmentation of innate host defenses against the invading hyphae, which in turn dampen immune responses. Factors in the tissue …

Risk factors for Mucormycosis

Risk factors for Mucormycosis

Risk factors for mucormycosis continued

Risk factors for mucormycosis continued

Mucormycosis

Review in @nejm.org by Dimitrios Kontoyiannis and Tom Walsh

www.nejm.org/doi/10.1056/...

#IDSky #TxID #MedMycoSky @msgerc.bsky.social

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Table of recommendations part 1

Table of recommendations part 1

Table of recommendations part 2

Table of recommendations part 2

Fungal diagnostic stewardship in immunocompromised populations: a focus on molds and dimorphic fungi

@jmsteinbrink.bsky.social @hannah-imlay.bsky.social et al on behalf of @msgerc.bsky.social

journals.asm.org/doi/10.1128/... #IDSky #MedMycoSky #MicroSky #TxID

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Schematic representation of iatrogenic mold central nervous system infections (1). The source of mold includes contamination during medication manufacturing, storage in a mold-contaminated environment, and environmental contamination during procedures (2). Routes of mold inoculation can occur in four situations: spinal puncture (epidural or spinal injection; most common), ventricular drainage devices (VP shunt or external ventricular device), transsphenoidal surgery, and craniotomy (3). Clinical complications of mold CNS infection include aneurysm formation, hemorrhagic stroke due to ruptured aneurysm, ischemic stroke, and meningoencephalitis.

Schematic representation of iatrogenic mold central nervous system infections (1). The source of mold includes contamination during medication manufacturing, storage in a mold-contaminated environment, and environmental contamination during procedures (2). Routes of mold inoculation can occur in four situations: spinal puncture (epidural or spinal injection; most common), ventricular drainage devices (VP shunt or external ventricular device), transsphenoidal surgery, and craniotomy (3). Clinical complications of mold CNS infection include aneurysm formation, hemorrhagic stroke due to ruptured aneurysm, ischemic stroke, and meningoencephalitis.

An unintended consequence: a review of iatrogenic central nervous system mold infections and outbreaks

Kontoyiannis and colleagues @msgerc.bsky.social
#IDSky #MedMycoSky

journals.asm.org/doi/10.1128/...

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We just published a new paper in Science Advances, where we uncover how #Candida albicans reprograms the metabolism of oral epithelial cells during infection.

As first and corresponding author, I’m excited to share what we found — and why it matters.

#Skytorial #Immunometabolism #MedMycoSky

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Algorithm for the management of suspected IC with septic shock. *For patients with IC who do not present with septic shock, empiric antifungal therapy should be withheld. In these cases, investigations should focus on obtaining blood cultures and, where relevant, site-directed samples. Biomarkers such as serum BDG may support discontinuation when suspicion decreases but should not be used as a trigger to initiate antifungal therapy. BDG (1 → 3)-β-D-glucan; IC Invasive candidiasis; R Resistance

Algorithm for the management of suspected IC with septic shock. *For patients with IC who do not present with septic shock, empiric antifungal therapy should be withheld. In these cases, investigations should focus on obtaining blood cultures and, where relevant, site-directed samples. Biomarkers such as serum BDG may support discontinuation when suspicion decreases but should not be used as a trigger to initiate antifungal therapy. BDG (1 → 3)-β-D-glucan; IC Invasive candidiasis; R Resistance

Table 5: Key actions in management of persistent candidemia

Table 5: Key actions in management of persistent candidemia

Table 6 Combination strategies for difficult deep-seated refractory infections. 
 Combination therapy is not routine. Reserve it for the specific scenarios above (endocarditis, CNS involvement, ocular disease, renal candidiasis with obstruction, persistent candidemia or very high fungal burden despite source control, suspected/proven resistance, major PK uncertainty or delayed TDM), begin with a pre-defined 48–72 h reassessment, obtain early susceptibility testing, perform TDM for azoles and consider it for echinocandins in complex PK settings, and de-escalate to the narrowest effective monotherapy as soon as feasible. In summary, avoid routine concurrent Amphotericin B–azole combinations for Candida spp. unless there is a compelling salvage reason; prefer alternative pairs (e.g., echinocandin + azole) if combination therapy is needed. If stepping from an azole to Amphotericin B, be aware of potential carry-over effects; if stepping from Amphotericin B to an azole, keep the overlap brief

Table 6 Combination strategies for difficult deep-seated refractory infections. Combination therapy is not routine. Reserve it for the specific scenarios above (endocarditis, CNS involvement, ocular disease, renal candidiasis with obstruction, persistent candidemia or very high fungal burden despite source control, suspected/proven resistance, major PK uncertainty or delayed TDM), begin with a pre-defined 48–72 h reassessment, obtain early susceptibility testing, perform TDM for azoles and consider it for echinocandins in complex PK settings, and de-escalate to the narrowest effective monotherapy as soon as feasible. In summary, avoid routine concurrent Amphotericin B–azole combinations for Candida spp. unless there is a compelling salvage reason; prefer alternative pairs (e.g., echinocandin + azole) if combination therapy is needed. If stepping from an azole to Amphotericin B, be aware of potential carry-over effects; if stepping from Amphotericin B to an azole, keep the overlap brief

Invasive candidiasis in intensive care medicine: shaping the future of diagnosis and therapy

Martin-Loeches et al, Intensive Care Medicine

link.springer.com/article/10.1... #IDSky #TxID #MedMycoSky

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New study shows antagonism between olorofim and voriconazole in vitro, suggesting this may be a class effect

academic.oup.com/jac/advance-... #MedMycoSky #TxID #IDSky

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ESCMID is looking to add officers to the Scientific Affairs Subcommittee with expertise in public health and Mycology respectively

Applicants from US, UK, Spain, China, Germany, Italy, Norway are excluded for reasons of geographic diversity/representation

#IDSky #MedMycoSky

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Visual abstract, featuring pie graph showing IFIs affecting 3.1% of the 1012 patients in the DESCART registry who had refractory/relapsed B cell lymphoma treated with CD19 CAR T cell therapy. The IFI related mortality among these 3.1% was 22%. Mostly candidemia and pulmonary aspergillosis, followed by Aspergillus/mucormycosis co-infection, PCP, and other.

Visual abstract, featuring pie graph showing IFIs affecting 3.1% of the 1012 patients in the DESCART registry who had refractory/relapsed B cell lymphoma treated with CD19 CAR T cell therapy. The IFI related mortality among these 3.1% was 22%. Mostly candidemia and pulmonary aspergillosis, followed by Aspergillus/mucormycosis co-infection, PCP, and other.

Invasive Fungal Infections after CD19 CAR T-cell Therapy for B-Cell Lymphoma: a LYSA study from the DESCAR-T Registry

IFI occurred in 3% of patients receiving CD19 CAR-T for refractory/relapsed B cell lymphoma

www.clinicalmicrobiologyandinfection.org/article/S119... #OpenAccess #MedMycoSky

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Nodule and histopathology in a case of Jorge Lobo’s disease in child with tick exposure, Brazil. A) Single granulomatous lesion on the right ear, which was surgically excised and histologically examined in 2018. B, C) Hematoxylin and eosin stain of nodule showing cells of the mononuclear phagocyte system, including monocytes, macrophages, epithelioid cells, and multinucleated giant cells, revealing granulomatous inflammation with spherical, double-walled yeast cells in branching chains (B) and prominent histiocytes and multinucleated giant cells (C), which are predominantly dense with areas of mild neovascularization, stromal hyalinization, and a slight infiltrate of lymphocytes and neutrophils. D) Grocott–Gomori methenamine silver stain of recurrent nodule from 2024 in which yeast-like fungal structures are diffusely distributed throughout the stroma and in the cytoplasm of phagocytic cells.

Nodule and histopathology in a case of Jorge Lobo’s disease in child with tick exposure, Brazil. A) Single granulomatous lesion on the right ear, which was surgically excised and histologically examined in 2018. B, C) Hematoxylin and eosin stain of nodule showing cells of the mononuclear phagocyte system, including monocytes, macrophages, epithelioid cells, and multinucleated giant cells, revealing granulomatous inflammation with spherical, double-walled yeast cells in branching chains (B) and prominent histiocytes and multinucleated giant cells (C), which are predominantly dense with areas of mild neovascularization, stromal hyalinization, and a slight infiltrate of lymphocytes and neutrophils. D) Grocott–Gomori methenamine silver stain of recurrent nodule from 2024 in which yeast-like fungal structures are diffusely distributed throughout the stroma and in the cytoplasm of phagocytic cells.

Lobomycosis

-caused by the noncultivable fungus, Paracoccidioides lobogeorgii (formerly Lacazia loboi)
-Found in Amazon basin
-causes keloid-like lesions
-Dx: histopath (round yeasts like pearls)

Here, a child developed it after a tick bite 1 yr earlier

wwwnc.cdc.gov/eid/article/... #MedMycoSky

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Preview
Medical cannabis as the source of Cryptococcus neoformans infection Abstract. Whole genome sequencing demonstrated Cryptococcus neoformans serotype A from cerebrospinal fluid and larynx of a patient receiving therapy for re

Medical cannabis as the source of Cryptococcus neoformans infection

Editor's Choice

Hong Nguyễn's team at @idpittstop.bsky.social

#OpenAccess #MedMycoSky #IDSky #TxID

academic.oup.com/cid/advance-...

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Preview
Weekly Screening of Circulating Mucorales DNA and early treatment in Severely Burned Patients Improves Survival: Real-Life Bi-center Experience in France Early serum Mucorales DNA detection in severely burned patients enables faster diagnosis of invasive wound mucormycosis, reducing 100-day mortality, partic

Weekly Screening of Circulating Mucorales DNA and early
treatment in Severely Burned Patients Improves Survival:
Real-Life Bi-center Experience in France

Emmanuale Faure... Alexandre Alanio and @sarah-delliere.bsky.social 

#IDSky #MedMycoSky #IDDx

academic.oup.com/cid/advance-...

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Post image

The #TxID team is growing and thriving! Grateful for this dedicated group—most pictured here—working to keep our transplant patients safe. Here’s to collaboration, curiosity, and camaraderie . 🌱🧬🦠 #IDSky #IDOnc #MedSky #MedMycoSky #ViroSky

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@idsainfo.bsky.social
@astct.bsky.social

#TxID
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#ViroSky
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Health risks with environmental changes and mould exposure. Key impacts of flooding include increased precipitation, rising sea levels and land use changes, leading to indoor mould growth and health risks such as respiratory issues, asthma exacerbation and mould infections. Case studies highlight varying health outcomes from Hurricane Katrina and Rita (2005), Colorado Flood (2013) and Hurricane Harvey (2017).

Health risks with environmental changes and mould exposure. Key impacts of flooding include increased precipitation, rising sea levels and land use changes, leading to indoor mould growth and health risks such as respiratory issues, asthma exacerbation and mould infections. Case studies highlight varying health outcomes from Hurricane Katrina and Rita (2005), Colorado Flood (2013) and Hurricane Harvey (2017).

Drivers of emerging fungal pathogens in a changing world. Climate change factors, such as rising temperatures and increasing resistance to fungicides, enhance fungal thermotolerance and drive the emergence of pathogens. Social determinants, including urbanisation, global travel and limited healthcare access, heighten human vulnerability to fungal infections. Other contributing factors, like environmental niches and unconfirmed environmental sources, further support the spread and persistence of fungal pathogens. These drivers contribute to the emergence of pathogens like Candida auris, Candida orthopsilosis and Cryptococcus deuterogatii.

Drivers of emerging fungal pathogens in a changing world. Climate change factors, such as rising temperatures and increasing resistance to fungicides, enhance fungal thermotolerance and drive the emergence of pathogens. Social determinants, including urbanisation, global travel and limited healthcare access, heighten human vulnerability to fungal infections. Other contributing factors, like environmental niches and unconfirmed environmental sources, further support the spread and persistence of fungal pathogens. These drivers contribute to the emergence of pathogens like Candida auris, Candida orthopsilosis and Cryptococcus deuterogatii.

Climate change and antifungal resistance: key mechanisms and pathogen examples. Climate change drives the development of antifungal resistance through mechanisms such as environmental pollution with fungicides, prolonged heat stress and increased mutation rates in fungi. These conditions promote genetic mutations, increased resistance to antifungal drugs and more challenging infections in humans and plants

Climate change and antifungal resistance: key mechanisms and pathogen examples. Climate change drives the development of antifungal resistance through mechanisms such as environmental pollution with fungicides, prolonged heat stress and increased mutation rates in fungi. These conditions promote genetic mutations, increased resistance to antifungal drugs and more challenging infections in humans and plants

Climate change: shifting boundaries of fungal disease in Europe and beyond

New review in Thorax

by @mbottery.bsky.social Sarah Sedik @germhuntermd.bsky.social @martinhoenigl.bsky.social @normanvanrhijn.bsky.social

thorax.bmj.com/content/thor... #MedSky #IDSky #PulmSky #ClimateSky #MedMycoSky

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Candida Endocarditis: current perspectives on diagnosis and therapy Candida infective endocarditis (CIE) is a rare but potentially devastating condition. Although it accounts for only 1-1.5% of infective endocarditis cases, CIE carries a high mortality rate (36-49%) a...

Candida Endocarditis: current perspectives on diagnosis and therapy

Ben-Ami Ronen, Bassetti Matteo, Bouza Emilio, Kosman Alex, Vena Antonio on behalf of @efisg-escmid.bsky.social

www.clinicalmicrobiologyandinfection.com/article/S119... #MedMycoSky #IDSky

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Are you interested in fungus-host interactions in the skin? Then, this postdoc position may be of interest to you 👇
#MedMycoSky #MicroSky

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Please share:
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#IDSky #HIVSky #MedMycoSky #MedSky

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Outcome predictors of Candida prosthetic joint infections: a systematic review and meta-analysis

DAIR associated w/ failure (0.25, 0.11-0.55, p<0.001), 1st-line AmB assoc w/ success (3.18, 1.25-9.87, p=0.014)

academic.oup.com/ofid/article... #MedMycoSky

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