Candidiasis, Chronic Mucocutaneous
Candidiasis, Cutaneous
Polyendocrinopathies, Autoimmune
Candidiasis
Candida albicans
Leishmaniasis, Mucocutaneous
Candidiasis, Oral
Interleukin-17
STAT1 Transcription Factor
Candidiasis, Invasive
Characterization of the cellular immune function of patients with chronic mucocutaneous candidiasis. (1/47)
Chronic mucocutaneous candidiasis (CMC) is a rare syndrome characterized by persistent and refractory infections of the skin, nails and mucosal tissues by yeasts of the genus Candida. Defects in the cellular limb of the immune system are well documented in CMC patients, but non-specific immune defects, such as myeloperoxidase deficiency or phagocyte chemotaxis disorders, have also been described. Nonetheless, the underlying defect(s) remains poorly understood, and further studies are required. We studied eight CMC patients without endocrinopathies, who showed (i) low normal proliferative response to phytohaemagglutinin (PHA), (ii) partially defective response to pokeweed mitogen (PWM), and (iii) impaired response to Candida and PPD antigens. Furthermore, peripheral blood mononuclear cells (PBMC) from CMC patients produced lower levels of type-1 cytokines (IL-2 and interferon-gamma) in response to Candida antigens, compared with control individuals. Conversely, we did not observe an enhancement of IL-4 and IL-10 in the patients, suggesting that, even though Th1 cytokines are decreased, the Th2 response is not increased in CMC. Nevertheless, the synthesis of these cytokines was normal when induced by PHA. We also observed an increased antigen-induced apoptosis in lymphocytes from the patients compared with controls, and this applied both to Candida and PPD antigens. Lastly, innate immunity defects were investigated. We observed an impairment of natural killer activity against K-562 target cells in half of the studied patients. These findings corroborate the extensive clinical and laboratory variability of CMC, which requires further studies on a larger number of patients to be better understood. (+info)An immune defect causing dominant chronic mucocutaneous candidiasis and thyroid disease maps to chromosome 2p in a single family. (2/47)
We describe a large family in which a combination of chronic mucocutaneous candidiasis (fungal infections of the skin, nails, and mucous membranes) and thyroid disease segregate as an autosomal dominant trait with reduced penetrance. The family includes (a) four members with both candidiasis and thyroid disease, (b) five members, including one pair of phenotype-concordant MZ twins, with candidiasis only, and (c) three members with thyroid disease only. A whole-genome scan using DNA samples from 20 members of the family identified a candidate linkage region on chromosome 2p. By sampling additional individuals and genotyping supplementary markers, we established linkage to a region of approximately 15 cM bounded by D2S367 and D2S2240 and including seven adjacent markers consistent with linkage. With a penetrance estimate of.8, which was based on pedigree and affected status, the peak two-point LOD score was 3.70 with marker D2S2328, and the peak three-point LOD score was 3.82. This is the first linkage assignment of a dominant locus for mucocutaneous candidiasis. (+info)Efficacy of ravuconazole in treatment of mucosal candidosis in SCID mice. (3/47)
A model of orogastric candidosis in SCID mice, which mimics disease seen in AIDS patients, was used to evaluate ravuconazole in comparison with fluconazole for treatment. Mice were infected orally with Candida albicans and received either no treatment or oral treatment once daily for 12 days with 1, 5, or 25 mg of ravuconazole per kg of body weight per day, 5 or 25 mg of fluconazole per kg per day, or diluent (10% dimethyl sulfoxide in 0.5% carboxymethyl cellulose). The numbers of C. albicans CFU in the esophagus, stomach, small intestine, and cecum on day 25 in mice given no treatment and diluent were equivalent. Both doses of fluconazole significantly reduced numbers of CFU in all four tissues but were equivalent to each other. Ravuconazole showed dose-responsive improvement of clearance of CFU. Ravuconazole at 25 mg/kg was superior in reduction of numbers of CFU in all tissues to controls or 25 mg of fluconazole per kg and to other regimens in at least three tissues. Fluconazole at 25 mg/kg cured no infection in any tissue, whereas 25 mg of ravuconazole/kg cleared infection in all tissues from 50% of mice. Ravuconazole has good efficacy and the potential to cure mucosal candidosis in the absence of a functional immune response. (+info)Early membrane exposure of phosphatidylserine followed by late necrosis in murine macrophages induced by Candida albicans from an HIV-infected individual. (4/47)
The hypothesis that Candida albicans isolate (CR1) from an HIV-infected individual induced apoptosis of macrophages was examined by optical microscopy, binding of annexin V-FITC and analyses of DNA degradation (TUNEL tests and agarose gel electrophoresis). Resident murine peritoneal macrophages co-incubated for 5-15 min with C. albicans CR1 bound annexin V, whereas macrophages incubated with either heat-inactivated strain CR1, C. albicans 577 (isolated from a patient with mucocutaneous candidiasis) or C. albicans FCF14 (a mutant that did not produce proteases and phospholipases) did not bind annexin for up to 2 h of observation. However, macrophages exposed to C. albicans CR1 did not present the pattern of DNA degradation typical of apoptosis. Macrophages became increasingly permeable to propidium iodide from 30 min to 2 h after their exposure to C. albicans CR1. Most of the phagocytosed C. albicans CR1 yeast cells switched to germ-tubes inside the macrophages after incubation for 1-2 h. These results show that macrophages exposed to C. albicans CR1 presented early signs of apoptosis but progressed to necrosis, and suggest that Candida strains that readily switch to germ-tubes inside those apoptotic cells might have a competitive advantage in vivo because released germ-tubes resist further attack by macrophages. (+info)A gene for familial isolated chronic nail candidiasis maps to chromosome 11p12-q12.1. (5/47)
Chronic mucocutaneous candidiases (CMC) are a group of rare disorders where an altered immune response against Candida leads to persistent and/or recurrent infections of the skin, nails, and mucous membranes. We analysed a five-generation Italian family with an isolated form of CMC, affecting nails only, in the presence of low serum concentration of intercellular adhesion molecule I (ICAM-1). We excluded linkage to candidate regions on chromosomes 2p (CMC with thyroid disease), 21q22.3 (APECED), and 19q13 (ICAM-1). We then carried out a genome-wide scan and assigned the CMC locus to a 19 cM pericentromeric region on chromosome 11. (+info)Deregulated production of protective cytokines in response to Candida albicans infection in patients with chronic mucocutaneous candidiasis. (6/47)
Patients with chronic mucocutaneous candidiasis (CMC) are selectively unable to clear the yeast Candida, which results in persistent debilitating infections affecting the skin, nails, and mucous membranes. The underlying defect is unknown. Recent animal studies highlighted the importance of type 1 cytokines in protection against Candida, and previous work suggested that CMC patients may exhibit altered cytokine production in response to Candida. Based on these findings, in this study we investigated cytokine production in CMC patients by assessing a range of inflammatory, anti-inflammatory, type 1, and type 2 cytokines (interleukin-2 [IL-2], IL-4, IL-5, IL-6, IL-10, IL-12, gamma interferon [IFN-gamma], tumor necrosis factor alpha [TNF-alpha]) in whole-blood cultures in response to five different fractions of Candida albicans (carbohydrate, purified mannan, and protein-rich fractions, etc.), as well as non-Candida antigens. Our results demonstrate that cytokine production is deregulated in a Candida-specific way for some cytokines (IL-2, IL-10), is deregulated more generally for other cytokines (IL-12, IL-6, IFN-gamma), and is not markedly altered for still other cytokines (TNF-alpha, IL-4, IL-5). The most notable finding in CMC patients was the markedly impaired production of IL-12 in parallel with dramatically increased levels of IL-6 and IL-10 that occurred selectively in response to Candida. These results suggest that patients with CMC have impaired production of type 1-inducing cytokines (possibly a macrophage or dendritic cell defect?), which could result in an inability to mount protective cell-mediated responses and a failure to clear Candida. Continued tissue damage and inflammation may trigger production of high levels of inhibitory cytokines, such as the IL-10 production seen in our study, which would further reduce production of type 1-inducing cytokines in a positive feedback loop leading to persistent infection. (+info)Protein carbonyl group content in patients affected by familiar chronic nail candidiasis. (7/47)
Familiar chronic nail candidiasis (FCNC) is a rare disorder characterized by early-onset infections caused by different species of Candida, restricted to the nail of the hands and feet, and associated with a low serum concentration of intercellular adhesion molecule 1. Host defense mechanisms against candidiasis require the cooperation of many immune cells through several candidacidal mechanisms, including oxygen-dependent killing mechanisms, mediated by a superoxide anion radical myeloperoxidase--H2O2--halide system, and reactive nitrogen intermediates. We analyzed protein carbonyl groups (considered a useful marker of oxidative stress) in the serum of patients belonging to a five-generation Italian family with an isolated form of FCNC. Serum protein carbonyl groups in FCNC patients were significantly lower than those measured in healthy donors. Also, if this hypothesis is merely speculative, we could suggest that the decreased circulating level of protein carbonyl groups in these patients is not a marker of a lower oxidative stress condition, but might be linked to a lower protease activity. (+info)Candida-specific interferon-gamma deficiency and toll-like receptor polymorphisms in patients with chronic mucocutaneous candidiasis. (8/47)
Chronic mucocutaneous candidiasis (CMC) is a group of disorders, characterised by persistent mucocutaneous infections with Candida species. The underlying defect of CMC has not been elucidated, but a defective cytokine response may be involved. Therefore, we investigated whether an imbalance between IFNgamma and IL-10 may play a role in this disorder. We assessed the cytokine production in whole-blood cultures from CMC patients using Candida albicans, lipopolysaccharide and phytohaemagglutinin as stimuli. As the Toll-like receptors are important pattern recognition receptors for Candida species, we also investigated Toll-like receptor polymorphisms in these patients. Patients with CMC had a significantly decreased IFNgamma production when whole blood was stimulated with C. albicans (232 +/- 120 vs 2279 +/- 609 pg/ml, p<0.02). When stimulated with phytohaemagglutinin, the differences were not significant (3549 +/- 1320 vs 7631 +/- 1790 pg/ml). The Candida-stimulated production of IL-10 tended to be higher in CMC patients, whereas TNF and IL-1beta production were similar in patients and controls. Stimulation with LPS showed no differences in cytokine production between patients and controls. Two out of seven patients had the TLR4 Asp299Gly polymorphism and none had the TLR2 Arg677Trp polymorphism. These data support the hypothesis that deficient IFNgamma production is involved in the pathogenesis of CMC, whereas a role for genetic polymorphisms of Toll-like receptor 2 and 4 is not obvious in these patients. (+info)Symptoms:
* White patches or lesions on the tongue, inside the cheeks, on the gums, and on the skin folds of the neck, armpits, groin, and under the breasts
* Redness and inflammation around the affected areas
* Itching, burning sensations, and pain in the affected areas
* Thickening and discoloration of the nails
* Bad breath or a "furry" tongue
* Skin cracks and fissures
* Nail brittleness and breaking
Causes:
* Overgrowth of Candida fungus, which is normally present in the body
* Poor oral hygiene
* Smoking
* Diabetes
* Obesity
* Hormonal changes during pregnancy or menopause
* Weakened immune system
* Prolonged use of antibiotics or steroids
* Cancer treatment
Diagnosis:
* Physical examination and observation of the symptoms
* Skin scraping or biopsy to confirm the presence of Candida fungus
* Blood tests to rule out other conditions
Treatment:
* Antifungal medications, such as clotrimazole, miconazole, and terbinafine, to kill the fungus
* Good oral hygiene practices, such as brushing and flossing regularly
* Avoiding smoking and sugar-rich diet
* Keeping the skin dry and clean
* Wearing loose-fitting clothing to reduce skin irritation
* Using a medicated mouthwash to treat oral thrush
* In severe cases, hospitalization may be necessary for intravenous antifungal medication
It is important to note that these are general guidelines and the best course of treatment will depend on the severity and location of the infection. A healthcare professional should always be consulted for proper diagnosis and treatment.
The symptoms of candidiasis, cutaneous may include:
* Redness and swelling on the affected area
* Itching and burning sensation
* Thickening and discoloration of the skin
* Cracks or fissures in the skin
Candidiasis, cutaneous can be diagnosed through a physical examination and may require additional tests such as a skin scraping or biopsy to confirm the diagnosis. Treatment typically involves antifungal medications and good wound care. In severe cases, hospitalization may be required.
Prevention is key in avoiding candidiasis, cutaneous. Good hygiene practices such as frequent handwashing, keeping the skin clean and dry, and avoiding sharing personal items can help reduce the risk of infection. Additionally, managing underlying conditions such as diabetes and taking antibiotics only when necessary can also help prevent candidiasis, cutaneous.
The term "polyendocrinopathy" refers to the involvement of multiple endocrine glands, while "autoimmune" indicates that the disorder is caused by an abnormal immune response against the body's own tissues.
Examples of polyendocrinopathies, autoimmune include:
1. Type 1 diabetes with thyroiditis and adrenal insufficiency
2. Hashimoto's thyroiditis with hypophyseal and adrenal involvement
3. Addison's disease with hypothyroidism and hemolytic anemia
4. Autoimmune polyglandular syndrome type 1 (APS-1) with autoantibodies against multiple endocrine glands
5. Autoimmune polyglandular syndrome type 2 (APS-2) with autoantibodies against thyroid, adrenal, and gonadal glands.
The exact cause of polyendocrinopathies, autoimmune is not fully understood, but it is thought to involve a combination of genetic and environmental factors that trigger an abnormal immune response against endocrine tissues. Treatment varies depending on the specific disorder and may include hormone replacement therapy, immunosuppressive medications, and management of associated symptoms.
Types of candidiasis:
1. Vulvovaginal candidiasis (VVC): a common infection that affects the vagina and vulva; symptoms include itching, burning, and abnormal discharge.
2. Oral thrush (OT): an infection that affects the mouth, often seen in infants and people with weakened immune systems; symptoms include white patches on the tongue and inside the cheeks.
3. Invasive candidiasis (IC): a severe infection that can spread throughout the body, often seen in people with weakened immune systems, such as those with HIV/AIDS or undergoing chemotherapy; symptoms include fever, chills, and difficulty breathing.
4. Candidal balanitis: an infection of the foreskin and glans of the penis; symptoms include redness, swelling, and pain.
5. Diaper rash: a common skin infection that affects infants who wear diapers; symptoms include redness, swelling, and irritability.
Causes and risk factors:
1. Overgrowth of Candida fungus due to an imbalance of the normal flora.
2. Use of antibiotics or steroids that can disrupt the balance of the body's natural flora.
3. Weakened immune system, such as in people with HIV/AIDS or undergoing chemotherapy.
4. Poor hygiene and sanitation.
5. Diabetes mellitus.
6. Pregnancy.
7. Obesity.
Diagnosis:
1. Physical examination and medical history.
2. Microscopic examination of a scraping or biopsy specimen.
3. Cultures of skin, blood, or other body fluids.
4. Polymerase chain reaction (PCR) or other molecular diagnostic techniques to detect the presence of the fungus.
Treatment:
1. Topical antifungal medications, such as clotrimazole, miconazole, or terbinafine, applied directly to the affected area.
2. Oral antifungal medications, such as fluconazole or itraconazole, for more severe infections or those that do not respond to topical treatment.
3. Antibiotics if there is a secondary bacterial infection.
4. Supportive care, such as pain management and wound care.
5. Proper hygiene and sanitation practices.
6. In severe cases, hospitalization may be necessary for intravenous antifungal medications and close monitoring.
Prevention:
1. Practice good hygiene and sanitation.
2. Avoid sharing personal items, such as towels or clothing.
3. Wash hands before touching the affected area.
4. Keep the affected area clean and dry.
5. Use of antifungal powders or sprays on the affected area.
6. Avoid using harsh soaps or cleansers that can irritate the skin.
7. Wear shoes in public areas to prevent exposure to fungal spores.
8. Avoid sharing bathing or showering facilities with others.
9. Dry thoroughly after bathing or swimming.
10. Use of antifungal medications as a prophylactic measure in high-risk individuals, such as those with weakened immune systems.
It's important to note that the best treatment and prevention strategies will depend on the specific type of fungus causing the infection, as well as the severity and location of the infection. It is essential to consult a healthcare professional for proper diagnosis and treatment.
Symptoms of mucocutaneous leishmaniasis include:
* Ulcers on the face, mouth, or nose
* Nosebleeds
* Difficulty swallowing
* Skin lesions on the face, arms, or legs
* Fever
* Swelling of the liver or spleen
Mucocutaneous leishmaniasis can be diagnosed through a combination of physical examination, medical history, and laboratory tests such as polymerase chain reaction (PCR) or direct agglutination test (DAT).
Treatment for mucocutaneous leishmaniasis typically involves the use of antiparasitic medications such as miltefosine, amphotericin B, or pentavalent antimonials. In severe cases, surgical debridement of skin lesions may be necessary.
Preventive measures for mucocutaneous leishmaniasis include avoiding sandfly bites and using insecticides to control sandfly populations.
Prognosis for mucocutaneous leishmaniasis is generally good if treated promptly and effectively, but can be poor if left untreated or if there is significant damage to the mucous membranes or skin.
Mucocutaneous leishmaniasis is a rare form of leishmaniasis that affects both the mucous membranes and the skin, causing ulcers, nosebleeds, and skin lesions. Prompt treatment with antiparasitic medications can improve the prognosis. Preventive measures include avoiding sandfly bites and using insecticides to control sandfly populations.
The infection is usually caused by an overgrowth of Candida, which is a normal flora in the mouth, but can become pathogenic under certain conditions. Risk factors for developing OC include taking antibiotics, wearing dentures, pregnancy, diabetes, and HIV/AIDS.
OC can be diagnosed by examining the mouth and throat with a mirror and torch, as well as through laboratory tests such as cultures or PCR. Treatment typically involves antifungal medication, good oral hygiene practices, and addressing any underlying conditions. In severe cases, hospitalization may be necessary.
Preventative measures include practicing good oral hygiene, avoiding smoking, and managing any underlying medical conditions. In addition, early diagnosis and treatment can help prevent the infection from spreading to other parts of the body, such as the bloodstream or heart.
Causes:
The most common cause of candidiasis is an imbalance in the natural bacteria and yeast that live in and around the vagina. This imbalance can be caused by a variety of factors, including:
* Taking antibiotics, which can kill off the "good" bacteria that keep candida in check
* Pregnancy and menopause, when hormonal changes can lead to an overgrowth of yeast
* Diabetes, which can cause excess sugar in the body that feeds the growth of yeast
* Weakened immune system
* Poor hygiene or poor fitting clothing and underwear that can trap moisture and create a warm environment for yeast to grow.
Symptoms:
The symptoms of candidiasis can vary from person to person, but common signs include:
* Itching, burning, and redness of the vulva and vagina
* A thick, white discharge that looks like cottage cheese and has no odor or a mild, sweet smell
* Pain or discomfort during sex
* Difficulty getting pregnant (infertility) if the infection is severe or recurrent.
Diagnosis:
A healthcare provider can diagnose candidiasis by performing a physical examination and taking a sample of vaginal discharge for testing. The provider may also take a culture of the yeast to determine which type of candida is causing the infection.
Treatment:
Candidiasis can be treated with antifungal medications, such as clotrimazole or terconazole. These medications are available over-the-counter or by prescription and come in creams, tablets, or suppositories. To help clear the infection, treatment may also include:
* Avoiding irritants such as douches, powders, or scented soaps
* Wearing loose-fitting clothing and cotton underwear
* Keeping the genital area clean and dry
* Avoiding sex during treatment
Complications:
If left untreated, candidiasis can lead to complications such as:
* Recurrent infections
* Inflammation of the vulva (vulvodynia)
* Inflammation of the vagina (vaginitis)
* Pain during sex
* Difficulty getting pregnant (infertility)
Prevention:
To prevent candidiasis, women can take the following steps:
* Practice good hygiene by washing the genital area gently with soap and water
* Avoid using douches, powders, or scented soaps
* Wear loose-fitting clothing and cotton underwear
* Change out of wet or sweaty clothes as soon as possible
* Avoid sex during treatment for candidiasis.
Prognosis:
With proper treatment, the prognosis for candidiasis is good. The infection usually clears up within a week or two with antifungal medication. However, recurrent infections can be more difficult to treat and may require longer courses of therapy. In some cases, candidiasis can lead to complications such as inflammation of the vulva or vagina, which can be more challenging to treat.
It is important for women to seek medical attention if they experience any symptoms of candidiasis, as early diagnosis and treatment can help prevent complications and improve outcomes.
Candidiasis, invasive is caused by the overgrowth of Candida in the body, which can occur for a variety of reasons, such as:
* Weakened immune system due to HIV/AIDS, cancer, or medications that suppress the immune system.
* Invasive medical devices, such as central lines or implanted pacemakers.
* Previous history of invasive candidiasis.
* Pregnancy.
* Intravenous drug use.
The symptoms of candidiasis, invasive can vary depending on the organs affected, but may include:
* Fever.
* Chills.
* Shortness of breath.
* Pain in the abdomen or chest.
* Confusion or disorientation.
* Skin rash or lesions.
Diagnosis of candidiasis, invasive is based on a combination of physical examination, medical history, and laboratory tests, such as blood cultures and imaging studies. Treatment typically involves the use of antifungal medications, which may be given intravenously or orally, depending on the severity of the infection. In severe cases, hospitalization may be necessary to monitor and treat the infection.
Prevention of candidiasis, invasive includes:
* Proper hygiene and handwashing practices.
* Avoiding close contact with individuals who have invasive candidiasis.
* Avoiding sharing of personal items, such as toothbrushes or razors.
* Avoiding the use of invasive medical devices, if possible.
* Proper care and maintenance of medical devices.
* Monitoring for signs of infection in individuals with weakened immune systems.
In conclusion, candidiasis, invasive is a serious and potentially life-threatening fungal infection that can affect various organs and systems in the body. Early diagnosis and treatment are crucial to prevent complications and improve outcomes. Proper prevention and control measures can help reduce the risk of developing invasive candidiasis.
Chronic mucocutaneous candidiasis
List of OMIM disorder codes
Interleukin 12
Autoimmune polyendocrine syndrome type 1
Interleukin-17 receptor
Oral candidiasis
STAT1
WHO disease staging system for HIV infection and disease
Immune dysregulation
Jane Aronson
CARD9
Angular cheilitis
Autoimmunity
Immunodeficiency
Autoimmune regulator
Mihai Netea
Bare lymphocyte syndrome type II
List of MeSH codes (C01)
CMC
Oral mucosa
John Raymond Hobbs
Addison's disease
Candidiasis
List of primary immunodeficiencies
List of MeSH codes (C17)
WHO Disease Staging System for HIV Infection and Disease in Adults and Adolescents
Thymic epithelial cell
Edouard Drouhet
Pemphigus vulgaris
Pruritus ani
List of skin conditions
Candida tropicalis
Mouth ulcer
Athlete's foot
Chronic mucocutaneous candidiasis: characterization of a family with STAT-1 gain-of-function and development of anex-vivoassay...
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Appendix F Unrelated Operating Room Procedures (MS-DRGs 981-989
Cutaneous candidiasis2
- Cutaneous candidiasis and other forms of candidiasis are infections caused by the yeast Candida albicans or other Candida species. (medscape.com)
- Superficial infections of skin and mucous membranes are the most common types of cutaneous candidiasis. (medscape.com)
Mucosal candidiasis2
- There have been significant changes in the management of candidiasis in the last few years, particularly related to the appropriate use of echinocandins and expanded-spectrum azoles for candidemia, other forms of invasive candidiasis, and mucosal candidiasis. (medscape.com)
- Also see the articles Mucosal Candidiasis and Candidiasis . (medscape.com)
Fungal8
- Patients with or without inherited or acquired abnormalities of immune function manifesting mucocutaneous and/or invasive fungal infections are eligible for screening and assessment under this protocol. (nih.gov)
- Adults or children (regardless of age, gender or ethnicity/race) with a known or yet uncharacterized inherited immunodeficiency and a definitively diagnosed mucocutaneous or invasive fungal infection. (nih.gov)
- Adults or children (regardless of age, gender or ethnicity/race) with acquired immunodeficiency and a severe, unusual, persistent or treatment-refractory chronic mucocutaneous fungal infection. (nih.gov)
- Adults or children (regardless of age, gender or ethnicity/race) with a well-documented prior, unusual, severe, persistent, or treatment-refractory mucocutaneous or invasive fungal infection(s), who have clinically recovered from the fungal infection. (nih.gov)
- Patients with abnormalities of immune function as manifested by recurrent or unusual fungal infections, recurrent or chronic inflammation, or previous laboratory evidence of immune dysfunction are eligible for screening and assessment under this protocol. (nih.gov)
- http://www.medscape.com/viewarticle/860442 LOS ANGELES Antifungal therapy relieves symptoms in patients with severe asthma, chronic sinusitis, or both whose sputum tests positive for fungal cultures, new research shows. (curezone.com)
- These results suggest that Ly6G+ G-MDSC-mediated TII is induced by either the i.p. and i.v. route of inoculation and protects against IAI or BSI forms of systemic candidiasis, with survival correlating with amelioration of sepsis and reduced organ-specific fungal burden. (bvsalud.org)
- Using an established A/J mouse model of disseminated infection that mimics human candidiasis, we showed that C3.1, a mAb that targets ß-1,2-mannotriose (ß-Man3), significantly extended survival and reduced fungal burdens in target organs, compared to control mice. (bvsalud.org)
Vulvovaginal Candidiasis4
- What is Vulvovaginal Candidiasis? (medscape.com)
- This is called a vulvovaginal candidiasis (VVC) infection or "yeast infection. (medscape.com)
- Cite this: Vulvovaginal Candidiasis - Medscape - Apr 29, 2010. (medscape.com)
- Clinical evaluation of recurrent episodes of vulvovaginal candidiasis is critical. (aafp.org)
Lichen Planus1
- Lichen planus is an inflammatory mucocutaneous condition with a distinctive appearance. (aafp.org)
Candidemia2
- The parenteral formulation is still under investigation for the treatment of candidemia and invasive candidiasis. (medscape.com)
- [ 46 ] Rezafungin is a long-acting echinocandin given wekly is being studied for candidemia and invasive candidiasis. (medscape.com)
Autoimmune3
- Adults or children (regardless of age, gender or ethnicity/race) with confirmed or suspected autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) who have not yet developed CMC. (nih.gov)
- Autoimmune polyendocrine syndrome type 1 (APS-1), or autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy is a rare, autosomal recessive autoimmune disease caused by a mutation of the autoimmune regulator ( AIRE ) gene. (e-apem.org)
- Autoimmune polyendocrine syndrome type 1 (APS-1), or autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (OMIM 240300), is a rare autosomal recessive autoimmune disease. (e-apem.org)
Hypoparathyroidism3
- The main symptom triad in APS-1 comprises chronic mucocutaneous candidiasis, adrenal insufficiency, and hypoparathyroidism. (e-apem.org)
- APS-1 is clinically diagnosed by the presence of at least 2 symptoms in the classic triad, as follows: chronic mucocutaneous candidiasis, adrenal insufficiency (Addison disease), and hypoparathyroidism. (e-apem.org)
- 1.46 mmol/L). Causes include chronic kidney disease, hypoparathyroidism, and metabolic or respiratory acidosis. (merckmanuals.com)
Candida1
- Candidiasis (Mucocutaneous) Candidiasis is skin and mucous membrane infection with Candida species, most commonly Candida albicans . (merckmanuals.com)
Systemic2
- Oropharyngeal candidiasis OPC can be treated with either topical antifungal agents (eg, nystatin, clotrimazole, amphotericin B oral suspension) or systemic oral azoles (fluconazole, itraconazole, or posaconazole). (medscape.com)
- Chronic mucocutaneous candidiasis, pancytopenia, and systemic mycosis in a patient with STAT1 gene mutation ineffectively treated with ruxolitinib. (krakow.pl)
Oropharyngeal1
- Current indications for the oral lozenges are as treatment or prevention of oropharyngeal candidiasis (oral thrush). (nih.gov)
Infections2
- Oral mucocutaneous lesions include chronic canker sores, herpes simplex virus, or any number of candidiasis infections. (uthscsa.edu)
- Known as chronic mucocutaneous candidiasis disease (CMCD), the condition causes persistent yeast (and sometimes bacterial) infections in the mouth, genitals, skin and fingernails. (nih.gov)
Mucous membranes1
- A clinical syndrome characterized by development, usually in infancy or childhood, of a chronic, often widespread candidiasis of skin, nails, and mucous membranes. (nih.gov)
Adrenal1
- This patient's main clinical manifestations were adrenal insufficiency and chronic mucocutaneous candidiasis. (e-apem.org)
Oral2
- Newer investigational agents already in clinical trials include ibrexafungerp, a glucan-synthase inhibitor, that was approved in 2021 for the treatment of vulvo-vaginal candidiasis in oral formulation. (medscape.com)
- Top services: Treatment of canker sores, oral lesions, Candidiasis and Sjogren's Syndrome. (uthscsa.edu)
Patients3
- Long-term therapy of chronic mucocutaneous candidiasis with ketoconazole: experience with twenty-one patients. (nih.gov)
- This type of finding may have an impact on future treatment recommendations and strategies of drug use for invasive candidiasis in different groups of patients. (medscape.com)
- The Extended Clinical Phenotype of 26 Patients with Chronic Mucocutaneous Candidiasis due to Gain-of-Function Mutations in STAT1. (cdc.gov)
Clinical1
- A revision of data outcomes on treatment of invasive candidiasis in clinical trials appears to favor use of echinocandins in terms of increased rate of survival. (medscape.com)
Asthma1
- Antifungals May Relieve Asthma, Chronic Sinusiti. (curezone.com)
Diseases2
- http://nationalpainreport.com/sibo-the-missing-piece-of-chronic-pain-dysautonomia-8832039.html SIBO, The Missing Piece of Chronic Pain Dysautonomia Posted on November 16, 2016 in Diseases & Conditions, Fibromyalgia, My Story with 10 Comments by Suzanne B. Stewart Suzanne B. Stewart One Summer day in 2002, a man ran through a red light and changed my life forever. (curezone.com)
- http://www.news.cornell.edu/stories/2016/06/indicator-chronic-fatigue-syndrome-found-gut-bacteria National Institute of Allergy and Infectious Diseases, National Institutes of Health Physicians have been mystified by chronic fatigue syndrome, a condition where normal exertion leads to debilitating fatigue that isn t alleviated by rest. (curezone.com)
Syndrome1
- The type II syndrome differs from type I in that it is associated with HLA-A1 and B8 haplotypes, onset is usually in adulthood, and candidiasis is not present. (wakehealth.edu)
Treatment1
- People ages 18 to 75 years with chronic mucocutaneous candidiasis who are not responding to standard non-intravenous treatment may be eligible to participate. (nih.gov)
Case1
- Ketoconazole in a case of chronic mucocutaneous candidiasis. (nih.gov)
Therapy1
- 15. [Practical management of side effects of tyrosine kinase inhibitor therapy in chronic myeloid leukemia]. (nih.gov)
Pain1
- After the MVA, I went through multiple surgeries, chronic intractable pain and then one medical issue/diagnosis after another. (curezone.com)
Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy7
- Perheentupa J. Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy. (medscape.com)
- Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy: report of seven additional sicilian patients and overview of the overall series from sicily. (medscape.com)
- Dermatological manifestations of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome. (medscape.com)
- No racial predilection is reported for chronic mucocutaneous candidiasis (CMC) , although autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is most prevalent in Finnish, Sardinian, and Iranian Jewish populations. (medscape.com)
- Other individuals have syndromes such as autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) or autosomal dominant hyper-IgE syndrome (AD-HIES) that include a tendency to develop candidiasis along with other signs and symptoms affecting various organs and systems of the body. (medlineplus.gov)
- Adults or children (regardless of age, gender or ethnicity/race) with confirmed or suspected autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) who have not yet developed CMC. (nih.gov)
- More than 90 mutations in the AIRE gene have been identified in people with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED). (nih.gov)
APECED1
- Chronic mucocutaneous candidiasis in APECED or thymoma patients correlates with autoimmunity to Th17-associated cytokines. (medscape.com)
Dystrophy1
- Candida organisms can also cause onychomycosis, including total nail dystrophy due to chronic mucocutaneous candidiasis (CMCC), a rare T-cell disorder. (medscape.com)
Autosomal dominant3
- STAT1 mutations in autosomal dominant chronic mucocutaneous candidiasis. (medscape.com)
- Autosomal Dominant Cases of Chronic Mucocutaneous Candidiasis Segregates with Mutations of Signal Transducer and Activator of Transcription 1, But Not of Toll-Like Receptor 3. (medscape.com)
- Autosomal-dominant chronic mucocutaneous candidiasis with STAT1-mutation can be complicated with chronic active hepatitis and hypothyroidism. (medscape.com)
Albicans2
- C albicans is the predominant causal organism of most candidiasis. (medscape.com)
- These experiments of nature indicate that human IL-17A and IL-17F are essential for mucocutaneous immunity against C. albicans, but otherwise largely redundant. (bvsalud.org)
CARD91
- only CARD9 gene mutations have also been known to lead to systemic candidiasis in some affected individuals. (medlineplus.gov)
Fungal infections3
- Candidiasis describes a group of fungal infections involving the skin and mucous membranes. (medscape.com)
- Patients with abnormalities of immune function as manifested by recurrent or unusual fungal infections, recurrent or chronic inflammation, or previous laboratory evidence of immune dysfunction are eligible for screening and assessment under this protocol. (nih.gov)
- Patients with or without inherited or acquired abnormalities of immune function manifesting mucocutaneous and/or invasive fungal infections are eligible for screening and assessment under this protocol. (nih.gov)
Heterogeneous group1
- CMCC is a heterogeneous group of disorders characterized by chronic candidal infections of the nails, skin, and mucous membranes. (medscape.com)
Mutations2
- Mutations in any of several genes have been identified in people with familial candidiasis. (medlineplus.gov)
- The gene mutations associated with familial candidiasis interfere with the IL-17 pathway in various ways. (medlineplus.gov)
Thrush1
- Thrush, or oral candidiasis, is also common in infants. (medscape.com)
Immunity4
- Inborn errors of human IL-17 immunity underlie chronic mucocutaneous candidiasis. (medscape.com)
- [ 1 , 2 ] Patients who lack T-cell immunity (eg, those with severe combined immune deficiency syndrome or DiGeorge syndrome) or patients with severely impaired T-cell function (eg, patients with AIDS) are susceptible to chronic candidal infections. (medscape.com)
- Defects in humoral immunity are not commonly observed in patients with CMC, and patients with antibody deficiencies are not particularly prone to candidiasis. (medscape.com)
- Chronic mucocutaneous candidiasis in humans with inborn errors of interleukin-17 immunity. (bvsalud.org)
Case of chronic2
Mucosal3
- Mucosal candidiasis. (medscape.com)
- The mucosal surfaces primarily affected by candidiasis are the oral cavity, esophagus, angles of the mouth, and genitals (causing vulvovaginitis in females, balanitis in males). (medscape.com)
- Patients should be counseled about smoking, and they should be warned about the risk of developing mucosal candidiasis after taking medications that impair salivation, antibiotics, corticosteroids, and other immunosuppressants. (medscape.com)
Mucous2
- however, the significant morbidity is related to chronic and persistent skin, nail, and mucous membrane candidal infections. (medscape.com)
- A clinical syndrome characterized by development, usually in infancy or childhood, of a chronic, often widespread candidiasis of skin, nails, and mucous membranes. (bvsalud.org)
Immunology1
- Lilic D. New perspectives on the immunology of chronic mucocutaneous candidiasis. (medscape.com)
Syndromes1
- This can lead to syndromes such as chronic mucocutaneous candidiasis (CMC). (medscape.com)
Immune3
- An immune defect causing dominant chronic mucocutaneous candidiasis and thyroid disease maps to chromosome 2p in a single family. (medscape.com)
- Some individuals experience recurrent candidiasis as part of a general susceptibility to infections because their immune systems are impaired by a disease such as acquired immune deficiency syndrome (AIDS) or severe combined immunodeficiency (SCID), medications, or other factors. (medlineplus.gov)
- The genes associated with familial candidiasis provide instructions for making proteins that are involved in immune system function. (medlineplus.gov)
Predilection1
- No gender predilection is noted in other forms of candidiasis. (medscape.com)
Nails1
- Candidiasis of the nails can result in thick, cracked, and discolored nails and swelling and redness of the surrounding skin. (medlineplus.gov)
Persistent3
- Women with familial candidiasis can develop frequent vaginal yeast infections, and infants can have yeast infections on the skin that cause persistent diaper rash. (medlineplus.gov)
- Adults or children (regardless of age, gender or ethnicity/race) with acquired immunodeficiency and a severe, unusual, persistent or treatment-refractory chronic mucocutaneous fungal infection. (nih.gov)
- Adults or children (regardless of age, gender or ethnicity/race) with a well-documented prior, unusual, severe, persistent, or treatment-refractory mucocutaneous or invasive fungal infection(s), who have clinically recovered from the fungal infection. (nih.gov)
Invasive2
- Adults or children (regardless of age, gender or ethnicity/race) with a known or yet uncharacterized inherited immunodeficiency and a definitively diagnosed mucocutaneous or invasive fungal infection. (nih.gov)
- 6. Efficacy of anidulafungin, caspofungin and fluconazole in the early phase of infection in a neutropenic murine invasive candidiasis model. (nih.gov)
Disease4
- Life expectancy is generally normal but significant morbidity is associated with the chronic nail and mucocutaneous infections and associated endocrine and/or autoimmune disease. (medscape.com)
- and (5) the significant cost of the procedure which could be as much as $250,000, not including the possible long-term care for chronic graft-versus-host disease. (nih.gov)
- Chronic granulomatous disease is characterized by white blood cells that cannot produce activated oxygen compounds and by defects in phagocytic cell microbicidal function. (msdmanuals.com)
- Chronic granulomatous disease usually begins with recurrent abscesses during early childhood, but in a few patients, onset is delayed until the early teens. (msdmanuals.com)
Syndrome2
- Autoimmunity and cystatin SA1 deficiency behind chronic mucocutaneous candidiasis in autoimmune polyendocrine syndrome type 1. (medscape.com)
- Autoantibodies against IL-17A, IL-17F, and IL-22 in patients with chronic mucocutaneous candidiasis and autoimmune polyendocrine syndrome type I. J Exp Med . (medscape.com)
Acute2
- Oral candidiasis may present as either white or erythematous lesions and either an acute or chronic infection. (medscape.com)
- 14. Salvage therapy of refractory chronic disseminated candidiasis in a patient with acute myeloid leukaemia and secondary prophylaxis during allogeneic stem cell transplantation. (nih.gov)
Oral3
- Oral candidiasis may also be an adverse effect from using inhaled corticosteroids for asthma due to oral deposition. (medscape.com)
- Oral candidiasis may predispose individuals to esophageal spread. (medscape.com)
- Candidiasis is seen in people with altered ecology, which in oral cases can be attributed to dental appliances, xerostomia, antimicrobials, nasopharyngeal steroids, oral cancer, or inflammatory diseases of the oral mucosa (e.g. pemphigus vulgaris). (medscape.com)
People1
- People ages 18 to 75 years with chronic mucocutaneous candidiasis who are not responding to standard non-intravenous treatment may be eligible to participate. (nih.gov)