The epidemiology of N. bracarensis needs to be better studied, as it is a recently described species that is phenotypically indistinguishable from N. glabratus and requires molecular methods for identification. However, some studies have reported the prevalence of N. bracarensis in different regions and clinical settings.
N. bracarensis was first described in 2006 from clinical isolates in Portugal. It has also been detected in other countries, such as Canada, USA, Spain, Italy, Japan, and Poland. The global prevalence of N. bracarensis among C. glabrata complex isolates has been estimated to range from 0.2% to 2.8%.
Most cases of N. bracarensis infection have been associated with bloodstream infection in immunocompromised patients, such as those with hematological malignancies, solid organ transplantation, or HIV infection. The symptoms may include fever, chills, hypotension, and organ dysfunction. The mortality rate there have been reports of bloodstream infections caused by N. bracarensis ranging from 25% to 50%.
It has shown variable susceptibility to antifungal agents, such as amphotericin B, fluconazole, voriconazole, posaconazole, itraconazole, anidulafungin, micafungin, and flucytosine2. Some isolates have been resistant to fluconazole and echinocandins. Therefore, antifungal susceptibility testing is recommended for optimal treatment of N. bracarensis infection.
Classification and Structure
Kingdom: Fungi
Division: Ascomycota
Class: Saccharomycetes
Order: Saccharomycetales
Family: Saccharomycetaceae
Genus: Nakaseomyces
Species: N. bracarensis
N. bracarensisis a type of yeast that belongs to the genus Nakaseomyces, which is closely related to Candida. Some possible points about its structure are:
N. bracarensis is an anamorphic yeast, which means it reproduces asexually by budding or fission.
N. bracarensis has a type strain of 153M T (=CBS 10154 T =NCYC D3853 T =CECT 12000 T), which is a reference strain that represents the species.
N. bracarensis has a circular genome of about 12.3 Mb, with 5,131 predicted genes and 13% GC content.
N. bracarensis has a cell wall composed of glucan, chitin, and mannoproteins, which helps it resist antifungal drugs and evade the host immune system.
N. bracarensis has a D1/D2 domain in its large subunit ribosomal RNA gene, which is used to identify and classify yeasts based on their sequence divergence.
Antigenic Types
The antigenic types of N. bracarensis have yet to be well known. Still, they may have some similarities with N. glabratus, which is a closely related species and a common cause of candidiasis in humans. N. glabratus expresses surface proteins called Epa (Epithelial adhesin) that mediate binding to host receptors and modulate the host response. These proteins are highly variable and may be involved in antigenic variation and immune evasion. N. glabratus also has a complex cell wall that contains different polysaccharides, such as β-glucans, mannans, and chitin. These components may also affect the antigenicity and immunogenicity of the yeast cells. N. bracarensis may have some or all these features, but more research is needed to confirm their role and relevance in human infections.
Pathogenesis
The pathogenesis of N. bracarensis and other Nocardia species involves several key steps:
Entry and colonization: Nocardia bacteria typically gain entry into the human body through inhalation of airborne spores or skin wounds. Once inside, they can establish a primary infection in the respiratory tract or at the site of injury.
Evasion of the immune system: Nocardia has several ways to avoid the immunological system of the host, including the ability to resist phagocytosis by macrophages. It helps the bacteria survive and multiply within host tissues.
Local infection and tissue damage: Nocardia can cause local tissue damage at the site of infection, resulting in the development of abscesses or granulomas. In the lungs, this can result in pneumonia with cavitation. It may result in the development of nodules or ulcers in the skin.
Dissemination: In some cases, Nocardia infections can disseminate to other parts of the body, leading to systemic nocardiosis. Dissemination occurs when the bacteria enter blood vessels and travel to other organs, such as the brain, liver, or kidneys. It can lead to severe and life-threatening infections.
Host factors: Host factors, such as underlying immunosuppression (e.g., in individuals with weakened immune systems due to conditions like HIV/AIDS, organ transplantation, or immunosuppressive medications), play a significant role in the pathogenesis of Nocardia infections. People whose immune systems are impaired are more prone to severe, widely spread diseases.
Host Defenses
The host defenses of N. bracarensis need to be better studied. Still, they may share some similarities with N. glabratus, which is known to have several mechanisms to evade or resist the immune system. Some of these mechanisms include:
Capacity to attach itself to and infiltrate epithelial cells, which may facilitate tissue damage and dissemination.
The expression of surface proteins called Epa (Epithelial adhesin) that mediate binding to host receptors and modulate the host response.
The production of extracellular phospholipases and aspartyl proteases that may contribute to tissue damage and inflammation.
The modification of the composition and structure of cell walls, which may affect the recognition and killing by phagocytes and the susceptibility to antifungal drugs.
The development of antifungal resistance through mutations in drug targets or efflux pumps.
These are some of the possible host defenses of N. bracarensis, but more research is needed to confirm their role and relevance in human infections.
Clinical manifestations
Nakaseomyces bracarensis is a type of yeast that can infect humans, particularly those with compromised immune systems. It is closely related to Nakaseomyces glabratus and Nakaseomyces nivariensis; these yeasts are often resistant to common antifungal drugs, making them difficult to treat.
Some of the symptoms of N. bracarensis infection may include:
Fever and chills
Skin rash or lesions
Oral thrush or white patches in the mouth
Vaginal discharge or itching
Burning during urinating or urinary tract infection
Bloodstream infection or sepsis
Meningitis is an inflammation of the membranes around the spinal cord and brain.
Endocarditis or infection of the heart valves
Osteomyelitis or infection of the bone
Diagnosis
The diagnosis of N. bracarensis is challenging, as it is phenotypically indistinguishable from N. glabratus, which is a closely related species and a common cause of candidiasis in humans. It is best identified by molecular methods or MALDI ToF MS, which can detect the sequence divergence in the D1/D2 domains of the 26S rRNA gene. Other methods, such as peptide nucleic acid fluorescence in situ hybridization (PNA-FISH), may also be helpful in differentiating N. bracarensis from N. glabratus. However, these methods are not widely available or standardized and may require further validation. Therefore, the diagnosis of N. bracarensis may be missed or delayed in clinical settings, which may have implications for the treatment and outcome of the infection.
Control
The prevention of N. bracarensis infection is like that of other Candida species, which are common causes of invasive candidiasis (IC) in immunocompromised and critically ill patients. Some of the general preventive measures include:
Reducing the use of broad-spectrum antibiotics, which may disrupt the normal flora and facilitate the overgrowth of Candida.
Avoiding the use of indwelling catheters or devices, which may serve as a source of contamination or biofilm formation by Candida.
Implementing strict infection control practices, such as hand hygiene, barrier precautions, and environmental cleaning, to prevent cross-transmission of Candida.
Monitoring the colonization and infection status of patients at risk, like those in critical care units (ICU), hematology and oncology wards, or those receiving immunosuppressive therapy.
Administering antifungal prophylaxis or pre-emptive therapy to selected high-risk patients based on local epidemiology, risk factors, and susceptibility patterns.
The epidemiology of N. bracarensis needs to be better studied, as it is a recently described species that is phenotypically indistinguishable from N. glabratus and requires molecular methods for identification. However, some studies have reported the prevalence of N. bracarensis in different regions and clinical settings.
N. bracarensis was first described in 2006 from clinical isolates in Portugal. It has also been detected in other countries, such as Canada, USA, Spain, Italy, Japan, and Poland. The global prevalence of N. bracarensis among C. glabrata complex isolates has been estimated to range from 0.2% to 2.8%.
Most cases of N. bracarensis infection have been associated with bloodstream infection in immunocompromised patients, such as those with hematological malignancies, solid organ transplantation, or HIV infection. The symptoms may include fever, chills, hypotension, and organ dysfunction. The mortality rate there have been reports of bloodstream infections caused by N. bracarensis ranging from 25% to 50%.
It has shown variable susceptibility to antifungal agents, such as amphotericin B, fluconazole, voriconazole, posaconazole, itraconazole, anidulafungin, micafungin, and flucytosine2. Some isolates have been resistant to fluconazole and echinocandins. Therefore, antifungal susceptibility testing is recommended for optimal treatment of N. bracarensis infection.
Classification and Structure
Kingdom: Fungi
Division: Ascomycota
Class: Saccharomycetes
Order: Saccharomycetales
Family: Saccharomycetaceae
Genus: Nakaseomyces
Species: N. bracarensis
N. bracarensisis a type of yeast that belongs to the genus Nakaseomyces, which is closely related to Candida. Some possible points about its structure are:
N. bracarensis is an anamorphic yeast, which means it reproduces asexually by budding or fission.
N. bracarensis has a type strain of 153M T (=CBS 10154 T =NCYC D3853 T =CECT 12000 T), which is a reference strain that represents the species.
N. bracarensis has a circular genome of about 12.3 Mb, with 5,131 predicted genes and 13% GC content.
N. bracarensis has a cell wall composed of glucan, chitin, and mannoproteins, which helps it resist antifungal drugs and evade the host immune system.
N. bracarensis has a D1/D2 domain in its large subunit ribosomal RNA gene, which is used to identify and classify yeasts based on their sequence divergence.
Antigenic Types
The antigenic types of N. bracarensis have yet to be well known. Still, they may have some similarities with N. glabratus, which is a closely related species and a common cause of candidiasis in humans. N. glabratus expresses surface proteins called Epa (Epithelial adhesin) that mediate binding to host receptors and modulate the host response. These proteins are highly variable and may be involved in antigenic variation and immune evasion. N. glabratus also has a complex cell wall that contains different polysaccharides, such as β-glucans, mannans, and chitin. These components may also affect the antigenicity and immunogenicity of the yeast cells. N. bracarensis may have some or all these features, but more research is needed to confirm their role and relevance in human infections.
Pathogenesis
The pathogenesis of N. bracarensis and other Nocardia species involves several key steps:
Entry and colonization: Nocardia bacteria typically gain entry into the human body through inhalation of airborne spores or skin wounds. Once inside, they can establish a primary infection in the respiratory tract or at the site of injury.
Evasion of the immune system: Nocardia has several ways to avoid the immunological system of the host, including the ability to resist phagocytosis by macrophages. It helps the bacteria survive and multiply within host tissues.
Local infection and tissue damage: Nocardia can cause local tissue damage at the site of infection, resulting in the development of abscesses or granulomas. In the lungs, this can result in pneumonia with cavitation. It may result in the development of nodules or ulcers in the skin.
Dissemination: In some cases, Nocardia infections can disseminate to other parts of the body, leading to systemic nocardiosis. Dissemination occurs when the bacteria enter blood vessels and travel to other organs, such as the brain, liver, or kidneys. It can lead to severe and life-threatening infections.
Host factors: Host factors, such as underlying immunosuppression (e.g., in individuals with weakened immune systems due to conditions like HIV/AIDS, organ transplantation, or immunosuppressive medications), play a significant role in the pathogenesis of Nocardia infections. People whose immune systems are impaired are more prone to severe, widely spread diseases.
Host Defenses
The host defenses of N. bracarensis need to be better studied. Still, they may share some similarities with N. glabratus, which is known to have several mechanisms to evade or resist the immune system. Some of these mechanisms include:
Capacity to attach itself to and infiltrate epithelial cells, which may facilitate tissue damage and dissemination.
The expression of surface proteins called Epa (Epithelial adhesin) that mediate binding to host receptors and modulate the host response.
The production of extracellular phospholipases and aspartyl proteases that may contribute to tissue damage and inflammation.
The modification of the composition and structure of cell walls, which may affect the recognition and killing by phagocytes and the susceptibility to antifungal drugs.
The development of antifungal resistance through mutations in drug targets or efflux pumps.
These are some of the possible host defenses of N. bracarensis, but more research is needed to confirm their role and relevance in human infections.
Clinical manifestations
Nakaseomyces bracarensis is a type of yeast that can infect humans, particularly those with compromised immune systems. It is closely related to Nakaseomyces glabratus and Nakaseomyces nivariensis; these yeasts are often resistant to common antifungal drugs, making them difficult to treat.
Some of the symptoms of N. bracarensis infection may include:
Fever and chills
Skin rash or lesions
Oral thrush or white patches in the mouth
Vaginal discharge or itching
Burning during urinating or urinary tract infection
Bloodstream infection or sepsis
Meningitis is an inflammation of the membranes around the spinal cord and brain.
Endocarditis or infection of the heart valves
Osteomyelitis or infection of the bone
Diagnosis
The diagnosis of N. bracarensis is challenging, as it is phenotypically indistinguishable from N. glabratus, which is a closely related species and a common cause of candidiasis in humans. It is best identified by molecular methods or MALDI ToF MS, which can detect the sequence divergence in the D1/D2 domains of the 26S rRNA gene. Other methods, such as peptide nucleic acid fluorescence in situ hybridization (PNA-FISH), may also be helpful in differentiating N. bracarensis from N. glabratus. However, these methods are not widely available or standardized and may require further validation. Therefore, the diagnosis of N. bracarensis may be missed or delayed in clinical settings, which may have implications for the treatment and outcome of the infection.
Control
The prevention of N. bracarensis infection is like that of other Candida species, which are common causes of invasive candidiasis (IC) in immunocompromised and critically ill patients. Some of the general preventive measures include:
Reducing the use of broad-spectrum antibiotics, which may disrupt the normal flora and facilitate the overgrowth of Candida.
Avoiding the use of indwelling catheters or devices, which may serve as a source of contamination or biofilm formation by Candida.
Implementing strict infection control practices, such as hand hygiene, barrier precautions, and environmental cleaning, to prevent cross-transmission of Candida.
Monitoring the colonization and infection status of patients at risk, like those in critical care units (ICU), hematology and oncology wards, or those receiving immunosuppressive therapy.
Administering antifungal prophylaxis or pre-emptive therapy to selected high-risk patients based on local epidemiology, risk factors, and susceptibility patterns.
The epidemiology of N. bracarensis needs to be better studied, as it is a recently described species that is phenotypically indistinguishable from N. glabratus and requires molecular methods for identification. However, some studies have reported the prevalence of N. bracarensis in different regions and clinical settings.
N. bracarensis was first described in 2006 from clinical isolates in Portugal. It has also been detected in other countries, such as Canada, USA, Spain, Italy, Japan, and Poland. The global prevalence of N. bracarensis among C. glabrata complex isolates has been estimated to range from 0.2% to 2.8%.
Most cases of N. bracarensis infection have been associated with bloodstream infection in immunocompromised patients, such as those with hematological malignancies, solid organ transplantation, or HIV infection. The symptoms may include fever, chills, hypotension, and organ dysfunction. The mortality rate there have been reports of bloodstream infections caused by N. bracarensis ranging from 25% to 50%.
It has shown variable susceptibility to antifungal agents, such as amphotericin B, fluconazole, voriconazole, posaconazole, itraconazole, anidulafungin, micafungin, and flucytosine2. Some isolates have been resistant to fluconazole and echinocandins. Therefore, antifungal susceptibility testing is recommended for optimal treatment of N. bracarensis infection.
Classification and Structure
Kingdom: Fungi
Division: Ascomycota
Class: Saccharomycetes
Order: Saccharomycetales
Family: Saccharomycetaceae
Genus: Nakaseomyces
Species: N. bracarensis
N. bracarensisis a type of yeast that belongs to the genus Nakaseomyces, which is closely related to Candida. Some possible points about its structure are:
N. bracarensis is an anamorphic yeast, which means it reproduces asexually by budding or fission.
N. bracarensis has a type strain of 153M T (=CBS 10154 T =NCYC D3853 T =CECT 12000 T), which is a reference strain that represents the species.
N. bracarensis has a circular genome of about 12.3 Mb, with 5,131 predicted genes and 13% GC content.
N. bracarensis has a cell wall composed of glucan, chitin, and mannoproteins, which helps it resist antifungal drugs and evade the host immune system.
N. bracarensis has a D1/D2 domain in its large subunit ribosomal RNA gene, which is used to identify and classify yeasts based on their sequence divergence.
Antigenic Types
The antigenic types of N. bracarensis have yet to be well known. Still, they may have some similarities with N. glabratus, which is a closely related species and a common cause of candidiasis in humans. N. glabratus expresses surface proteins called Epa (Epithelial adhesin) that mediate binding to host receptors and modulate the host response. These proteins are highly variable and may be involved in antigenic variation and immune evasion. N. glabratus also has a complex cell wall that contains different polysaccharides, such as β-glucans, mannans, and chitin. These components may also affect the antigenicity and immunogenicity of the yeast cells. N. bracarensis may have some or all these features, but more research is needed to confirm their role and relevance in human infections.
Pathogenesis
The pathogenesis of N. bracarensis and other Nocardia species involves several key steps:
Entry and colonization: Nocardia bacteria typically gain entry into the human body through inhalation of airborne spores or skin wounds. Once inside, they can establish a primary infection in the respiratory tract or at the site of injury.
Evasion of the immune system: Nocardia has several ways to avoid the immunological system of the host, including the ability to resist phagocytosis by macrophages. It helps the bacteria survive and multiply within host tissues.
Local infection and tissue damage: Nocardia can cause local tissue damage at the site of infection, resulting in the development of abscesses or granulomas. In the lungs, this can result in pneumonia with cavitation. It may result in the development of nodules or ulcers in the skin.
Dissemination: In some cases, Nocardia infections can disseminate to other parts of the body, leading to systemic nocardiosis. Dissemination occurs when the bacteria enter blood vessels and travel to other organs, such as the brain, liver, or kidneys. It can lead to severe and life-threatening infections.
Host factors: Host factors, such as underlying immunosuppression (e.g., in individuals with weakened immune systems due to conditions like HIV/AIDS, organ transplantation, or immunosuppressive medications), play a significant role in the pathogenesis of Nocardia infections. People whose immune systems are impaired are more prone to severe, widely spread diseases.
Host Defenses
The host defenses of N. bracarensis need to be better studied. Still, they may share some similarities with N. glabratus, which is known to have several mechanisms to evade or resist the immune system. Some of these mechanisms include:
Capacity to attach itself to and infiltrate epithelial cells, which may facilitate tissue damage and dissemination.
The expression of surface proteins called Epa (Epithelial adhesin) that mediate binding to host receptors and modulate the host response.
The production of extracellular phospholipases and aspartyl proteases that may contribute to tissue damage and inflammation.
The modification of the composition and structure of cell walls, which may affect the recognition and killing by phagocytes and the susceptibility to antifungal drugs.
The development of antifungal resistance through mutations in drug targets or efflux pumps.
These are some of the possible host defenses of N. bracarensis, but more research is needed to confirm their role and relevance in human infections.
Clinical manifestations
Nakaseomyces bracarensis is a type of yeast that can infect humans, particularly those with compromised immune systems. It is closely related to Nakaseomyces glabratus and Nakaseomyces nivariensis; these yeasts are often resistant to common antifungal drugs, making them difficult to treat.
Some of the symptoms of N. bracarensis infection may include:
Fever and chills
Skin rash or lesions
Oral thrush or white patches in the mouth
Vaginal discharge or itching
Burning during urinating or urinary tract infection
Bloodstream infection or sepsis
Meningitis is an inflammation of the membranes around the spinal cord and brain.
Endocarditis or infection of the heart valves
Osteomyelitis or infection of the bone
Diagnosis
The diagnosis of N. bracarensis is challenging, as it is phenotypically indistinguishable from N. glabratus, which is a closely related species and a common cause of candidiasis in humans. It is best identified by molecular methods or MALDI ToF MS, which can detect the sequence divergence in the D1/D2 domains of the 26S rRNA gene. Other methods, such as peptide nucleic acid fluorescence in situ hybridization (PNA-FISH), may also be helpful in differentiating N. bracarensis from N. glabratus. However, these methods are not widely available or standardized and may require further validation. Therefore, the diagnosis of N. bracarensis may be missed or delayed in clinical settings, which may have implications for the treatment and outcome of the infection.
Control
The prevention of N. bracarensis infection is like that of other Candida species, which are common causes of invasive candidiasis (IC) in immunocompromised and critically ill patients. Some of the general preventive measures include:
Reducing the use of broad-spectrum antibiotics, which may disrupt the normal flora and facilitate the overgrowth of Candida.
Avoiding the use of indwelling catheters or devices, which may serve as a source of contamination or biofilm formation by Candida.
Implementing strict infection control practices, such as hand hygiene, barrier precautions, and environmental cleaning, to prevent cross-transmission of Candida.
Monitoring the colonization and infection status of patients at risk, like those in critical care units (ICU), hematology and oncology wards, or those receiving immunosuppressive therapy.
Administering antifungal prophylaxis or pre-emptive therapy to selected high-risk patients based on local epidemiology, risk factors, and susceptibility patterns.
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