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short note on Candida albicans
cryptococcus neoformans esa3
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Fungal infections are either opportunistic or endemic ubiquitous fungi that exist freely in the environment cause endemic fungal infections. On the other hand, opportunistic fungal infections only cause disease when the immune system degrades [1]. Opportunistic fungi are commensal with the host and a very low intrinsic virulence to cause until the immunity is altered. Some of these include: Candida species, Aspergillus species, pneumocystic jirovecii and Cyptococcus neoformans. These disseminate diseases such as: oral candidiasis (oral thrush), genito-urinary disease and ocular or sinus infections which may spread to involve the Central Nervous system [2]. Opportunistic fungal infections are mainly immunocompromised individuals such as: those with HIV, extensive surgery, haematological disorders, and those who have corticosteroids, cytotoxic and suppressive chemotherapy. As a result, their neutrophils drop to abnormal counts, a conditioning know as neutropenia. This state predisposes these patients to many opportunistic fungal infections such as: candidiasis, aspergillosis, cryptococcosis and pneumocystis among others [3].
Candidiasis is a common fungal infection in immunocompromised individuals caused by Candida albicans- a normal oral flora in the genitourinary tract, gastrointestinal tract and on the skin. It form bio films on any surface and cause both mucosal and systemic infections in immunocompromised hosts disseminated as: oral thrush, vulvovaginitis, endocarditis among others [15]. Although Candida albicans still remains the major cause of nosocomial infections, other non albicans candida species such as: Candida glabrata, Candida tropicalis and Candida parapsilosis are increasingly becoming common. Accordin...
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[33] M. A. Viviani, M. Cogliati, M. C. Esposto et al., “Molecular analysis of 311 Cryptococcus neoformans isolates from a 30- monthECMMsurveyofcryptococcosisinEurope,”FEMSYeast Research, vol. 6, no. 4, pp. 614–619, 2006.
[62] S. H. M. Chen, M. F. Stins, S. H. Huang et al., “Cryptococcus neoformans induces alterations in the cytoskeleton of human brainmicrovascularendothelialcells,”JournalofMedicalMicro- biology, vol. 52, no. 11, pp. 961–970, 2003.
[63] Y. C. Chang, M. F. Stins, M. J. McCaffery et al., “Cryptococcal yeast cells invade the central nervous system via transcellular penetrationoftheblood-brainbarrier,”InfectionandImmunity, vol. 72, pp. 4985–4995, 2004.
[64] M. Alvarezand A.Casadevall,“Phagosomeextrusionandhost- cell survival after Cryptococcus neoformans phagocytosis by macrophages,” Current Biology, vol. 16, no. 21, pp. 2161–2165, 2006
For medical care, no treatment is needed for those who are asymptomatic, just monitoring for mild symptoms (2). For those who cannot fight the disease as easily as the majority, there are an array of treatments available. To start, blood cultures should be performed in all patients, and sputum cultures should be taken for those with chronic histoplasmosis (2). Chest radiology would be preferred for individuals with acute pulmonary histoplasmosis, steroids and possible laser treatment for ocular histoplasmosis, and CT scans for those with cerebral histoplasmosis (2). With prolonged symptoms of more than 4 weeks, medical therapy via itraconazole is recommended for 6-12 weeks, followed by chest imaging (2). Bronchiectasis caused by the microbe is treated with either a bronchoscopy or surgical removal (3). Phrenological treatments to histoplasmosis include amphorcetericin B, ketoconazole, itraconazole, and fluconazole (3). Currently, antifungal agents are being developed to offer alternative treatment (3). To successfully survive as a pathogen, the virus must change itself on a micro level to survive changing conditions, macrophages, and other threats to the fungi’s reproduction (4). Being able to go from an environmental mold to an intercellular yeast is extremely useful for a microbe in an ecosystem that fights for control of those it infects (4). These advantages present within histoplasmosis are what keeps it as a cause of respiratory and systemic disease in mammals (4). There are plenty of treatments available to accommodate all forms of histoplasmosis, making it a microbe that is very simple to cure, despite how hard it tries to
Plenty of fungal problems exist, including athlete’s foot, jock itch, ringworm, and onychomycosis (fungal infection beneath nails). However, many antifungal drugs exist as well, such as Lamisil, which is the most effective. Using the molecule terbinafine hydrochloride, it puts holes in the cell membranes of fungal cells, and can destroy fungi. Despite this, Lamisil has many problems such as harmful side effects, and a high cost, and can therefore be vastly improved. Some of Lamisil’s competitors, such as Tinactin, offer a similar medication for a cheaper price, and other analogs of the drug could prove to be safer and even more effective. For now though, Lamisil, the 87th best selling prescription drug in the world, is the best antifungal medication1.
...ly 24 hours postinfection, during the late exponential and early stationary phases, SpeB is dramatically upregulated as tissue invasion occurs and the bacteria disseminate (13). It is speculated that this upregulation occurs so that SpeB can cleave the GAS adhesive molecules and allow the bacteria to spread throughout the tissue during invasive infections (20). Following the dissemination of GAS in this stage, SpeB expression is once again downregulated as the bacterium invades the bloodstream. GAS selects for mutations in the CovRS regulatory system, which result in reduced expression of SpeB and a simultaneous enhancement of the production of another virulence factor, Sda1. Sda1 helps avoid host neutrophil extracellular traps, allowing the bacterium to survive in the bloodstream and produce the bacteremia and sepsis characteristic of invasive GAS infections (26).
Microbiology with Diseases by Body System (Hardcover) & MasteringMicrobiology, 3rd edition, Bauman, R. W., Benjamin- Cummings Publishing Company, 2012, San Francisco, CA. ISBN 9780321716378. OR
This condition may be caused by a bacterial infection or infection with a parasite called an amoeba (Entamoeba histolytica). In rare cases, it can also be caused by infection with a fungus called Candida.
The yeast is already there. A number of factors can increase the chance of the yeast growing out of control. The leading cause is overuse of antibiotics. Yeast must compete for the right to live on us with various other organisms, many of them bacteria. These bacteria, which live on the skin and in the intestine and vagina, among other places, are harmless but good at fighting off yeast. When we take antibiotics to deal with less friendly bacteria, we kill off these harmless ones as well. Yeast, which is unaffected by antibiotics, moves into the vacated spots once occupied by bacteria, and starts to grow and
Candida albicans is a harmless commensal yeast which becomes pathogenic when environmental changes trigger the virulence factors of the organism. Hence Candida species are opportunistic pathogens in susceptible individuals. Oral infection caused by C. albicans known as oral candidiasis or candidosis. However, C. albicans exist in the mouths of 80% of healthy individuals. Any alteration in the environment of oral cavity can change the presence of candida from commensal to pathogenic. This translation in the status of candida is due to many predisposing factors. In the past, oral candidiasis was thought to affect mainly elderly and very young population. Recently, the incidence of oral candidiasis increased greatly with the intensification of HIV infection and immunosuppressive chemotherapy (1, 2). Oral candidiasis colonize 5% to 7% of newborn less than one month old. The infection also estimated to affect 9% to 31% of AIDS patients and nearly 20% of cancer patients (3). This review discuss the possible causes, the types of oral candidiasis, treatment and management strategies.
Streptococcus pneumoniae is a facultative anaerobe, which after performing a Gram-staining appears as blue-black cocci with the lancet shape, mostly in pair...
Infections tend to be mild and may cause flu-like symptoms. Many time, the infection will require an antifungal treatment (Kellner et al, 111). Because of the flu-like symptoms, this disease was fairly difficult to diagnose; many patients died and were thought to have died from the flu. In 1892, the disease was finally discovered, was originally recognized as Coccidioides immitis only, and was treated with antifungal drugs (Cox and Magee, 805). According to the initial, official studies of this disease, patients could live anywhere from four months to nine years. The first two patients were drastically different; patient one had a slowly progressing form of Coccidioidomycosis, the disease caused by both Coccidioides immitis and Coccidioides posadasii. Patient one lived for nine years after the initial diagnosis and never received any antifungal treatment (Cox and Magee, 806). Patient two had a much more rapidly progressing form of Coccidioidomycosis. Patient two lived for only four months and died from the infection caused by the Coccidioides immitis pathogen (Cox and Magee, 806). Patient one made those studying this disease because that the pathogen would be slow acting, so patient two was treated as though the pathogen wouldn’t take full effect for a few years. As stated above, Coccidioidomycosis is the disease caused by Coccidioides immitis and Coccidioides posadasii. Coccidioidomycosis
In order to infect the meninges, pathogens must cross the blood brain barrier. According to Myers, Director of Infection Control at Scripps Mercy hospital (2000), pathogens enter through an open wound, surgical incision, or a mucus membrane. Systemic infections can also result in meningitis (Huether & McCance, 2012) with typical invasion occurring through the middle ear or during respiratory tract infections (Myers, 2000). Bacteria elude the body’s immune defenses with their capsule; viruses hide within the body’s own cells and invade the cerebrospinal fluid through the cerebral capillary system (Myers, 2000).
Tettelin, H., Nelson, K. E., Paulsen, I. T., Eisen, J. A., Read, T. D., Peterson, S., et al. (2001). Complete genome sequence of a virulent isolate of Streptococcus pneumoniae. Science. Retrieved from http://www.sciencemag.org/content/293/5529/498.short (Accessed December 12, 2013).
Murray, Patrick R., Ken S. Rosenthal and Michael A. Pfaller. Medical Microbiology, 6th Edition. Philadelphia: Mosby Elsevier, 2009.
Mucor is a life-threatening fungal infection that occurs in immunocompromised patients and its caused by a group of molds called mucoromycetes. It’s mainly affects people with weakened immune systems and can occur in nearly any part of the body. These molds live throughout the environment. It most commonly affects the sinuses or the lungs after inhaling fungal spores from the air, or the skin after the fungus enters the skin through a cut, scrape, burn, or other type of skin trauma. Mucormycosis refers to several different diseases caused by infection with fungi in the order of Mucorales.
Pictures of yeast infection will make you want to think seriously about infection by fungus more specifically by yeast. Single celled, yeast is able to multiply and make your life a living hell. This description can only be confirmed by people who continue to suffer from new and recurring infections. There is general discomfort when you have yeast overgrowth and women tend to suffer more. You will find many pictures of the infection on the internet and some of the places or areas of the body you will get to view are the vagina, skin, gut, mouth and many more. You might find the pictures graphic and if you are not strong enough, they might be very disturbing.
I obtained my Ph.D. in micro/molecular biology from the Nickerson laboratory at the University of Nebraska-Lincoln, where I investigated pathogenic fungi Candida albicans morphogenesis, and host-fungal interactions. I discovered that upon being phagocytized by macrophages, C. albicans pierce the phagolysosome by inducing hyphae by up-regulating cAMP/PKA pathway. But, before dying, macrophages induce the expression of IL-6, IL-1beta, TNF-alpha, and IL-10, which help developing specific Th cells. While in the acidic conditions such as phagolysosome, C. albicans alters the production of quorum sensing molecules to reduce the acidic microenvironment as a survival strategy.