DOCSLIB.ORG

Interaction of Candida Albicans with Human Leukocytes and Serum'

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Interaction of Candida Albicans with Human Leukocytes and Serum' JOURNAL OF BACTERIOLOGY, June 1969, p. 996-1004 Vol. 98, No. 3 Copyright © 1969 American Society for Microbiology Printed in U.S.A. Interaction of Candida albicans with Human Leukocytes and Serum' ROBERT I. LEHRER AND MARTIN J. CLINE Cancer Research Institute and the Department of Medicine, University of California Medical Center, San Francisco, California 94122 Received for publication 10 January 1969 A quantitative assay of candidacidal activity based on differential staining of non- viable Candida albicans by methylene blue was developed and applied to studies of leukocytes from normal individuals and patients with fungal and other infections. Serum factors were necessary for optimal phagocytosis of C. albicans but lacked direct candidacidal activity. Normal human neutrophils (38 studies) killed 29.0 a 7.4% of ingested C. albicans in 1 hr. Eosinophils and monocytes killed a smaller percentage. Neutrophil candidacidal activity did not require protein or ribonucleic acid synthesis by the leukocyte but was inhibited by anaerobic conditions, potas- sium cyanide, and colchicine. Leukocytes of a patient with hereditary myeloperoxi- dase deficiency and of three children with chronic granulomatous disease phago- cytized C. albicans normally, yet failed to kill them. Our data suggest that the neutrophil can play an important role in resistance to Candida infection and that the lysosomal enzyme myeloperoxidase and its oxidant substrate hydrogen peroxide are the major participants in neutrophil candidacidal activity. Although certain disorders and therapeutic pro- on Sabouraud agar slants at room temperature and cedures appear to alter man's susceptibility to were transferred every 2 months. fungal infection, the factors involved in either Test organisms were inoculated into 50 ml of Sa- bouraud dextrose broth (Difco) and cultured or altered responses to fungal challenge 2% normal at 33 C. Under these conditions, the Candida cells are Candida albicans is incompletely defined. rep- grew only in yeast phase. Only cultures with fewer than resentative of the group of opportunistic patho- 5% nonviable organisms, as determined by dye exclu- gens which cause disease in the impaired host (3, sion (vide infra), were employed in assays. This condi- 5, 13, 44). This study was undertaken to develop a tion was fulfilled by most cultures 3 to 14 days old. quantitative method capable of measuring the Candida cells were quantitated in a hemocytometer candidacidal activity of human leukocytes and and resuspended in Hanks balanced salt solution serum and to define the metabolic pathways of (BSS) for use in candidacidal assays. the leukocyte which participate in the candidaci- Leukocyte preparation. Peripheral venous blood 5 units of per ml dal process. The new method and results of its containing heparin (Lilly, benzyl alcohol preservative) was mixed with half its volume application to studies of leukocyte function and of 3% dextran in normal saline (39) and allowed to simplified in vitro models of Candida infection sediment at room temperature for 30 to 45 min. The are presented. leukocyte-rich supernatant fluid was removed, cen- trifuged at 150 X g for 10 min, and washed twice MATERIALS AND METHODS with BSS containing 10% fetal calf serum and 5 units of heparin per ml. Leukocyte and absolute polymor- C. albicans. A strain of C. albicans (UC 820) was phonuclear (PMN) cell concentrations were deter- obtained from the Department of Clinical Pathology, mined by hemocytometer count. Just before being University of California. It showed features typical of forma- added to the assay, the leukocytes were centrifuged at C. albicans (2, 27), including chlamydospore 150 X g for 8 min and resuspended in BSS at a final tion, rapid filamentation in the presence of serum (38), concentration of 107 PMN/ml. Erythrocyte contami- on EMB characteristic growth pattern agar, fermenta- nation of the preparations was variable, usually ap- with acid and gas pro- tion of dextrose and maltose one red cell per white cell. Platelet con- and to proximating duction, lack of lactose fermentation, failure tamination also varied, but usually was less than one gas in sucrose. Stock cultures were maintained produce platelet per five leukocytes. Serum. Fresh serum was obtained from several I This work was presented in part at the 1968 Meeting of the American Federation for Clinical Research, Atlantic City, N.J. normal group AB donors, stored individually in 4-ml (Clin. Res. 16:331, 1968). volumes on dry ice, and used within 1 month. In some 996 VOL. 98, 1969 INTERACTION OF C. ALBICANS WITH HUMAN LEUKOCYTES 997 experiments leukocytes were studied in the donor again decanted and replaced with 1 ml of BSS con- patient's serum. taining 2 X 106 Candida cells and 25% normal AB Neutrophil candidacidal assay. Equal volumes (0.25 serum. After a 30-min incubation period, the mono- ml) of AB serum, leukocyte suspension, and BSS cytes were washed twice with warm BSS and serum to were added to sterile plastic tubes (12 by 75 mm). All remove the nonphagocytized yeast cells; they were tubes were prepared in duplicate; a third tube con- then incubated for an additional 60 min in fresh BSS taining all components except leukocytes served as a containing AB serum. In the tubes without cover slips, control. Sterile technique was used throughout. the incubation was terminated by the addition of The tubes were incubated for 10 min at 37 C. A 0.25 ml of 2.5% sodium deoxycholate (pH 8.7) to lyse 0.25-mi volume of C. albicans at a concentration of 107 the monocytes. Methylene blue was added, and the yeast cells per ml was then added, and the tubes were suspensions were handled and counted as in the neu- rotated (30 rev/min) at 37 C for 60 min. After 15 trophil assay. For assessment of phagocytosis, cover min, a drop was taken for direct examination and slips from the other Leighton tubes were stained and preparation of stained smears to confirm that all examined. added organisms had been ingested. At 60 min, 0.25 ml of 2.5% sodium deoxycholate (pH 8.7) was added RESULTS to each tube. At this concentration, deoxycholate causes immediate lysis of the blood cells without Differential staining of viable and nonviable damage to the Candida cells. Methylene blue, 0.01% Candida. We established the ability of methylene in distilled water, was then added to achieve a final blue to specifically stain nonviable C. albicans in volume of 4 to 5 ml and a final dye concentration of several ways. Usually, fewer than 5% of the cells about 0.0075% or 2 X 10-4 M. The Candida cell in the Candida broth cultures were stained by suspensions were centrifuged at 1,100 X g for 15 min 2 X 10-4 M methylene blue. If the yeast cells were at 4 C and resuspended in about 0.5 ml of the residual killed by boiling for 10 min, all were intensely supernatant fluid. Thereafter, the tubes were kept in stained. Staining occurred promptly and was in- an ice-water bath until they could be examined mi- dependent of pH in the of 5 to 8. A croscopically. At least 300 Candida cells from each range repre- tube were examined to determine the percentage sentative mixture of heat-killed and viable Can- stained. To derive the candidacidal activity due to the dida cells after exposure to 2 X 10-4 M methylene action of phagocytes, the percentage of stained yeast blue is shown in Fig. 1. cells in the control tubes, usually 0.5 to 2.5%, was The specificity of the methylene blue staining of subtracted from that in the experimental tubes. All phagocytized C. albicans cells was studied as tubes were counted in a "blind" manner to avoid follows. After an inoculum of Candida cells was subjective bias. ingested by normal leukocytes, the leukocytes Viable Candida cells, which were unstained, clearly were lysed with deoxycholate, and methylene blue differed from the nonviable organisms, which took a was added. A drop of the lysed uniform, intense blue cytoplasmic stain. If Candida suspension was cells were left at 0 C in the presence of methylene blue placed on a slide containing a thin strip of for more than 3 hr, some of the organisms acquired a Sabouraud agar, sealed with a cover slip, and diffuse, faintly blue tinge; therefore, observations were observed microscopically at intervals for 8 hr. concluded within this time period. During several such experiments, unstained Can- Candidacidal activity was independent of the Can- dida cells were seen to bud and form micro- dida-neutrophil ratio over a range of 0.5 to 1.5 Candida colonies, whereas the blue-stained Candida cells cells per neutrophil and of serum concentrations in the always failed to bud. range of 6 to 50%. When cells of C. albicans cultured The possibility that methylene blue was itself for 72 hr or more were used, no multiplication oc- responsible for killing the phagocytized Candida curred during the 60-min incubation period of the assay, ensuring that the percentage killed was directly cells that were stainable was excluded by the proportional to the absolute number killed. Initial ex- following experiment. Ingested Candida cells were periments revealed that leukocytes killed by repeated again recovered from normal leukocytes by de- freezing and thawing lacked candidacidal activity in oxycholate lysis and divided into duplicate por- this system. tions. One portion was diluted with Sabouraud Monocyte candidacidal assay. Monocytes were iso- broth, and pour plates were made in Sabouraud lated from heparinized peripheral blood of normal agar for colony counts. The second portion was donors by previously described methods (8) and diluted with 0.01 % methylene blue, and the con- suspended at 106 cells per ml in medium TC 199 con- centration of Candida cells was determined in a taining 30% fetal calf serum.
Load more

Recommended publications
  • Austin Ultrahealth Yeast-Free Protocol 1
    1 01/16/12/ Austin UltraHealth Yeast-Free Protocol 1. Follow the Yeast Diet in your binder for 6 weeks or you may also use recipes from the Elimination Diet. (Just decrease the amount of grains and fruits allowed). 2. You will be taking one pill of prescription antifungal daily, for 30 days. This should always be taken two hours away from your probiotics. This medication can be very hard on your liver so it is important to refrain from ALL alcohol while taking this medication. Candida Die-Off Some patients experience die-off symptoms while eliminating the yeast, or Candida, in their gut. Die off symptoms can include the following: Brain fog Dizziness Headache Floaters in the eyes Anxiety/Irritability Gas, bloating and/or flatulence Diarrhea or constipation Joint/muscle pain General malaise or exhaustion What Causes Die-Off Symptoms? The Candida “die-off” occurs when excess yeast in the body literally dies off. When this occurs, the dying yeasts produce toxins at a rate too fast for your body to process and eliminate. While these toxins are not lethal to the system, they can cause an increase in the symptoms you might already have been experiencing. As the body works to detoxify, those Candida die-off symptoms can emerge and last for a matter of days, or weeks. The two main factors which cause the unpleasant symptoms of Candida die off are dietary changes and antifungal treatments, both of which you will be doing. Dietary Changes: When you begin to make healthy changes in your diet, you begin to starve the excess yeasts that have been hanging around, using up the extra sugars in your blood.
    [Show full text]
  • Candida Auris
    microorganisms Review Candida auris: Epidemiology, Diagnosis, Pathogenesis, Antifungal Susceptibility, and Infection Control Measures to Combat the Spread of Infections in Healthcare Facilities Suhail Ahmad * and Wadha Alfouzan Department of Microbiology, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait; [email protected] * Correspondence: [email protected]; Tel.: +965-2463-6503 Abstract: Candida auris, a recently recognized, often multidrug-resistant yeast, has become a sig- nificant fungal pathogen due to its ability to cause invasive infections and outbreaks in healthcare facilities which have been difficult to control and treat. The extraordinary abilities of C. auris to easily contaminate the environment around colonized patients and persist for long periods have recently re- sulted in major outbreaks in many countries. C. auris resists elimination by robust cleaning and other decontamination procedures, likely due to the formation of ‘dry’ biofilms. Susceptible hospitalized patients, particularly those with multiple comorbidities in intensive care settings, acquire C. auris rather easily from close contact with C. auris-infected patients, their environment, or the equipment used on colonized patients, often with fatal consequences. This review highlights the lessons learned from recent studies on the epidemiology, diagnosis, pathogenesis, susceptibility, and molecular basis of resistance to antifungal drugs and infection control measures to combat the spread of C. auris Citation: Ahmad, S.; Alfouzan, W. Candida auris: Epidemiology, infections in healthcare facilities. Particular emphasis is given to interventions aiming to prevent new Diagnosis, Pathogenesis, Antifungal infections in healthcare facilities, including the screening of susceptible patients for colonization; the Susceptibility, and Infection Control cleaning and decontamination of the environment, equipment, and colonized patients; and successful Measures to Combat the Spread of approaches to identify and treat infected patients, particularly during outbreaks.
    [Show full text]
  • Candida Species Identification by NAA
    Candida Species Identification by NAA Background Vulvovaginal candidiasis (VVC) occurs as a result of displacement of the normal vaginal flora by species of the fungal genus Candida, predominantly Candida albicans. The usual presentation is irritation, itching, burning with urination, and thick, whitish discharge.1 VVC accounts for about 17% to 39% of vaginitis1, and most women will be diagnosed with VVC at least once during their childbearing years.2 In simplistic terms, VVC can be classified into uncomplicated or complicated presentations. Uncomplicated VVC is characterized by infrequent symptomatic episodes, mild to moderate symptoms, or C albicans infection occurring in nonpregnant and immunocompetent women.1 Complicated VVC, in contrast, is typified by severe symptoms, frequent recurrence, infection with Candida species other than C albicans, and/or occurrence during pregnancy or in women with immunosuppression or other medical conditions.1 Diagnosis and Treatment of VVC Traditional diagnosis of VVC is accomplished by either: (i) direct microscopic visualization of yeast-like cells with or without pseudohyphae; or (ii) isolation of Candida species by culture from a vaginal sample.1 Direct microscopy sensitivity is about 50%1 and does not provide a species identification, while cultures can have long turnaround times. Today, nucleic acid amplification-based (NAA) tests (eg, PCR) for Candida species can provide high-quality diagnostic information with quicker turnaround times and can also enable investigation of common potential etiologies
    [Show full text]
  • Candida & Nutrition
    Candida & Nutrition Presented by: Pennina Yasharpour, RDN, LDN Registered Dietitian Dickinson College Kline Annex Email: [email protected] What is Candida? • Candida is a type of yeast • Most common cause of fungal infections worldwide Candida albicans • Most common species of candida • C. albicans is part of the normal flora of the mucous membranes of the respiratory, gastrointestinal and female genital tracts. • Causes infections Candidiasis • Overgrowth of candida can cause superficial infections • Commonly known as a “yeast infection” • Mouth, skin, stomach, urinary tract, and vagina • Oropharyngeal candidiasis (thrush) • Oral infections, called oral thrush, are more common in infants, older adults, and people with weakened immune systems • Vulvovaginal candidiasis (vaginal yeast infection) • About 75% of women will get a vaginal yeast infection during their lifetime Causes of Candidiasis • Humans naturally have small amounts of Candida that live in the mouth, stomach, and vagina and don't cause any infections. • Candidiasis occurs when there's an overgrowth of the fungus RISK FACTORS WEAKENED ASSOCIATED IMUMUNE SYSTEM FACTORS • HIV/AIDS (Immunosuppression) • Infants • Diabetes • Elderly • Corticosteroid use • Antibiotic use • Contraceptives • Increased estrogen levels Type 2 Diabetes – Glucose in vaginal secretions promote Yeast growth. (overgrowth) Treatment • Antifungal medications • Oral rinses and tablets, vaginal tablets and suppositories, and creams. • For vaginal yeast infections, medications that are available over the counter include creams and suppositories, such as miconazole (Monistat), ticonazole (Vagistat), and clotrimazole (Gyne-Lotrimin). • Your doctor may prescribe a pill, fluconazole (Diflucan). The Candida Diet • Avoid carbohydrates: Supporters believe that Candida thrives on simple sugars and recommend removing them, along with low-fiber carbohydrates (eg, white bread).
    [Show full text]
  • GRAS Notice for Pichia Kudriavzevii ASCUSDY21 for Use As a Direct Fed Microbial in Dairy Cattle
    GRAS Notice for Pichia kudriavzevii ASCUSDY21 for Use as a Direct Fed Microbial in Dairy Cattle Prepared for: Division of Animal Feeds, (HFV-220) Center for Veterinary Medicine 7519 Standish Place Rockville, Maryland 20855 Submitted by: ASCUS Biosciences, Inc. 6450 Lusk Blvd Suite 209 San Diego, California 92121 GRAS Notice for Pichia kudriavzevii ASCUSDY21 for Use as a Direct Fed Microbial in Dairy Cattle TABLE OF CONTENTS PART 1 – SIGNED STATEMENTS AND CERTIFICATION ................................................................................... 9 1.1 Name and Address of Organization .............................................................................................. 9 1.2 Name of the Notified Substance ................................................................................................... 9 1.3 Intended Conditions of Use .......................................................................................................... 9 1.4 Statutory Basis for the Conclusion of GRAS Status ....................................................................... 9 1.5 Premarket Exception Status .......................................................................................................... 9 1.6 Availability of Information .......................................................................................................... 10 1.7 Freedom of Information Act, 5 U.S.C. 552 .................................................................................. 10 1.8 Certification ................................................................................................................................
    [Show full text]
  • Vaginal Yeast Infection a Vaginal Yeast Infection Is an Infection of the Vagina, Most Commonly Due to the Fungus Candida Albicans
    5285 Anthony Wayne Drive, Detroit, MI 48202 (P) 313-577-5041 | (F) 313-577-9581 health.wayne.edu Vaginal Yeast Infection A vaginal yeast infection is an infection of the vagina, most commonly due to the fungus Candida albicans. Causes, incidence, and risk factors Most women have a vaginal yeast infection at some time. Candida albicans is a common type of fungus. It is often found in small amounts in the vagina, mouth, digestive tracts, and on the skin. Usually it does not cause disease or symptoms. Candida and the many other germs that normally live in the vagina keep each other in balance. However, sometimes the number of Candida albicans increases, leading to a yeast infection. A yeast infection can happen if you are: • Taking antibiotics used to treat other types of infections. Antibiotics change the normal balance between germs in the vagina by decreasing the number of protective bacteria. • Pregnant • Obese • Have diabetes A yeast infection is not a sexually transmitted illness. However, some men will develop symptoms such as itching and a rash on the penis after having sexual contact with an infected partner. Having many vaginal yeast infections may be a sign of other health problems. Other vaginal infections and discharges can be mistaken for vaginal yeast infection. Symptoms • Pain with intercourse • Painful urination • Redness and swelling of the vulva • Vaginal and labial itching, burning • Abnormal Vaginal Discharge • Ranges from a slightly watery, white discharge to a thick, white, chunky discharge (like cottage cheese) Signs and Tests A pelvic examination will be done. It may show swelling and redness of the skin of the vulva, in the vagina, and on the cervix.
    [Show full text]
  • Targeting the Burkholderia Cepacia Complex
    viruses Review Advances in Phage Therapy: Targeting the Burkholderia cepacia Complex Philip Lauman and Jonathan J. Dennis * Department of Biological Sciences, University of Alberta, Edmonton, AB T6G 2E9, Canada; [email protected] * Correspondence: [email protected]; Tel.: +1-780-492-2529 Abstract: The increasing prevalence and worldwide distribution of multidrug-resistant bacterial pathogens is an imminent danger to public health and threatens virtually all aspects of modern medicine. Particularly concerning, yet insufficiently addressed, are the members of the Burkholderia cepacia complex (Bcc), a group of at least twenty opportunistic, hospital-transmitted, and notoriously drug-resistant species, which infect and cause morbidity in patients who are immunocompromised and those afflicted with chronic illnesses, including cystic fibrosis (CF) and chronic granulomatous disease (CGD). One potential solution to the antimicrobial resistance crisis is phage therapy—the use of phages for the treatment of bacterial infections. Although phage therapy has a long and somewhat checkered history, an impressive volume of modern research has been amassed in the past decades to show that when applied through specific, scientifically supported treatment strategies, phage therapy is highly efficacious and is a promising avenue against drug-resistant and difficult-to-treat pathogens, such as the Bcc. In this review, we discuss the clinical significance of the Bcc, the advantages of phage therapy, and the theoretical and clinical advancements made in phage therapy in general over the past decades, and apply these concepts specifically to the nascent, but growing and rapidly developing, field of Bcc phage therapy. Keywords: Burkholderia cepacia complex (Bcc); bacteria; pathogenesis; antibiotic resistance; bacterio- phages; phages; phage therapy; phage therapy treatment strategies; Bcc phage therapy Citation: Lauman, P.; Dennis, J.J.
    [Show full text]
  • Skin Immunity to Candida Albicans
    TREIMM 1284 No. of Pages 11 Feature Review Skin Immunity to Candida albicans Sakeen W. Kashem1 and Daniel H. Kaplan2,* Candida albicans is a dimorphic commensal fungus that colonizes healthy Trends human skin, mucosa, and the reproductive tract. C. albicans is also a predomi- Primary immunodeficiencies reveal nantly opportunistic fungal pathogen, leading to disease manifestations such as conserved IL-17 stimulating/signaling disseminated candidiasis and chronic mucocutaneous candidiasis (CMC). The pathways involved in mucocutaneous differing host susceptibilities for the sites of C. albicans infection have revealed defense against C. albicans. tissue compartmentalization with tailoring of immune responses based on the Mouse models have demonstrated site of infection. Furthermore, extensive studies of host genetics in rare cases of both innate and adaptive sources of IL-17 in response to C. albicans. CMC have identified conserved genetic pathways involved in immune recogni- tion and the response to the extracellular pathogen. We focus here on human Immunity against C. albicans is com- and mouse skin as a site of C. albicans infection, and we review established and partmentalized towards sites of infection. newly discovered insights into the cellular pathways that promote cutaneous antifungal immunity. Non-hematopoietic cells provide anti- fungal immunity in the skin. Compartmentalization of Immunity Against C. albicans Skin Infection C. albicans is the most common and well-studied of the disease-causing Candida spp., and naturally colonizes the skin, genital, and/or intestinal mucosa in up to 70% of healthy individuals [1]. Under normal circumstances, the fungus does not cause disease but the absence of appropriate immune recognition and response mechanisms can lead to the inability to control C.
    [Show full text]
  • Yeast Infection Division of Disease Control What Do I Need to Know?
    Division of Disease Control What Do I Need To Know? Yeast Infection (Thrush, Diaper Rash, Vaginitis) What is a yeast infection? Yeast infections are caused by a fungus called Candida albicans. These infections can present in a variety of forms. Yeast infections in women can infect the vagina, called vaginitis. Thrush causes mouth infections in young infants and can also be a presenting sign of HIV infection in adults. Candida also may be the cause of many types of diaper rash in young children. Who is at risk for a yeast infection? Anyone can get a yeast infection. What are the symptoms of a yeast infection? Candidia diaper rash: The diaper area is red. The redness is worse in the creases. Redness is often bordered by red pimples. Rash may have a shiny appearance. Sores or cracking or oozing is present in severe cases. Thrush White patches appear on the inside of cheeks and gums and tongue. Thrush usually causes no other signs or symptoms. Vaginitis Vaginal irritation, intense itchiness and vaginal discharge. How soon do symptoms appear? Incubation period is unknown. How is a yeast infection spread? The fungus is present in the intestinal tract and mucous membranes of healthy people. A warm environment allows for growth and spread. Page 1 of 2 Last Updated: 01/2016 Person-to-person transmission may occur from a woman to her infant when the mother has a yeast infection in her vagina and in breastfeeding mothers whose babies with thrush infect the mothers’ nipples. When and for how long is a person able to spread the disease? A person can spread disease as long as the infection is present.
    [Show full text]
  • Yeast Infection (Candidiasis)
    PROVIDER YEAST INFECTION (CANDIDIASIS) Candida can normally be found on the skin and in the mouth, throat, intestinal tract, and vagina of healthy people. In children, yeast infections are commonly found in the mouth or throat (thrush) or the diaper area. CAUSE Candida albicans, a fungus. SYMPTOMS Thrush - White, slightly raised patches on the tongue or inside the cheek. Diaper Rash - Smooth, shiny "fire engine" red rash with a raised border. Children who suck their thumbs or fingers may occasionally develop Candida infections around their fingernails. Under certain conditions, such as during antibiotic use or when skin is damaged and exposed to excessive moisture, the balance of the normal, healthy skin germs is upset. Therefore, yeast that normally live on the skin can overgrow and cause yeast infections. Most of the time these infections heal quickly, but sometimes illness can occur in infants, persons with weakened immune systems, or those taking certain antibiotics. SPREAD Rarely, by contact with skin lesions and mouth secretions of infected persons or asymptomatic carriers. Most infants who have Candida got it from their mother during childbirth. According to the Centers for Disease Control and Prevention, outbreaks of thrush in childcare settings may be the result of increased use of antibiotics rather than newly acquired Candida infections. INCUBATION Variable. For thrush in infants, it usually takes 2 to 5 days. For others, yeast infections may occur while taking antibiotics or shortly after stopping the antibiotics. CONTAGIOUS Contagious while lesions are present. Most infections occur from yeast in the PERIOD person’s own body. DIAGNOSIS Recommend parents/guardians call their healthcare provider to identify the fungus.
    [Show full text]
  • Candida Auris: a Drug-Resistant Germ That Spreads in Healthcare Facilities
    Candida auris: A drug-resistant germ that spreads in healthcare facilities Candida auris (also called C. auris) is a fungus that causes serious infections. Patients with C. auris infection, their family members and other close contacts, public health officials, laboratory staff, and healthcare workers can all help stop it from spreading. Why is Candida auris a problem? It causes serious infections. C. auris can cause bloodstream infections and even death, particularly in hospital and nursing home patients with serious medical problems. More than 1 in 3 patients with invasive C. auris infection (for example, an infection that affects the blood, heart, or brain) die. It’s often resistant to medicines. Antifungal medicines commonly used to treat Candida infections often don’t work for Candida auris. Some C. auris infections have been resistant to all three types of antifungal medicines. It’s becoming more common. Although C. auris was just discovered in 2009, it has spread quickly and caused infections in more than a dozen countries. It’s difficult to identify. C. auris can be misidentified as other types of fungi unless specialized laboratory technology is used. This misidentification might lead to a patient getting the wrong treatment. It can spread in hospitals and nursing homes. C. auris has caused outbreaks in healthcare facilities and can spread through contact with affected patients and contaminated surfaces or equipment. Good hand hygiene and cleaning in healthcare facilities is important because C. auris can live on surfaces for several weeks. How do I know if I have a Candida Most people who get auris infection? serious Candida infections C.
    [Show full text]
  • Candida and Candidiasis—Opportunism Versus Pathogenicity: a Review of the Virulence Traits
    microorganisms Review Candida and Candidiasis—Opportunism Versus Pathogenicity: A Review of the Virulence Traits Cristina Nicoleta Ciurea 1,2,* , Irina-Bianca Kosovski 2,3, Anca Delia Mare 1, Felicia Toma 1, Ionela Anca Pintea-Simon 1,2 and Adrian Man 1 1 Department of Microbiology, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mures, , 540139 Târgu Mures, , Romania; [email protected] (A.D.M.); [email protected] (F.T.); [email protected] (I.A.P.-S.); [email protected] (A.M.) 2 Doctoral School, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mures, , 540139 Târgu Mures, , Romania; [email protected] 3 Department of Physiopathology, George Emil Palade University of Medicine, Pharmacy, Science, and Technology of Târgu Mures, , 540139 Târgu Mures, , Romania * Correspondence: [email protected] Received: 7 May 2020; Accepted: 4 June 2020; Published: 6 June 2020 Abstract: One of the most important questions in microbiology nowadays, is how apparently harmless, commensal yeasts like Candida spp. can cause a rising number of infections. The occurrence of the disease requires firstly the attachment to the host cells, followed by the invasion of the tissue. The adaptability translates into a rapid ability to respond to stress factors, to take up nutrients or to multiply under different conditions. By forming complex intracellular networks such as biofilms, Candida spp. become not only more refractive to antifungal therapies but also more prone to cause disease. The inter-microbial interactions can enhance the virulence of a strain. In vivo, the fungal cells face a multitude of challenges and, as a result, they develop complex strategies serving one ultimate goal: survival.
    [Show full text]