Microbiology Research Paper Free Essays

string(50) " along with several other species of trypanosoma\." African Trypanosomiasis, also known as â€Å"sleeping sickness†, is a parasitic disease of people and animals caused by microscopic parasites of the species Trypanosoma brucei. It is transmitted by the tsetse fly, which is found only in rural Africa. Although the infection is not found in the United States, historically, it has been a serious public health problem in some regions of sub-Saharan Africa covering about 37 countries and 60 million people (African Trypanosomiasis [also known as Sleeping Sickness] 2010). We will write a custom essay sample on Microbiology Research Paper or any similar topic only for you Order Now The term â€Å"sleeping sickness† was given primarily because when infected, invasion of the cerebrospinal fluid and brain after infection of the blood is often delayed, resulting in symptoms of extreme fatigue that can last for several years before the severe phase of the disease sets in; toxemia, coma and death (Trypanosomiasis, African 2009). With the huge number of people it affects, it is weird that I only discovered it now when faced with a microorganism research paper. The glaring explanation behind this, is that there are many much larger, deadlier diseases in Africa, that ultimately make diseases like sleeping sickness get overlooked. This may be true, but that is no reason not to pay attention to a disease like this because it has and does affect and kill thousands of people. When researching this topic many questions arose and they were all addressed with further research. Things addressed in this paper are: how many people the disease effects annually, the cure for humans infected with the organism, where in the world people are affected, whether the number of infections is increasing or decreasing, the side effects when a human is infected, the impact on the economy if there was to be an outbreak, the kinds of treatment given to those who are infected, the future plans for the infection, the comparison of infections in third world countries to first world, and the long lasting effects the disease can leave after treatment. Most speculation and hype related to diseases in Africa focus on malaria and AIDS, but while researching Sleeping Sickness it is clear that there are many more large scale, but less known, diseases affecting the population of Africa. I was really hoping to learn more about the issues that come up when trying to treat a large number of people in a country like Africa where disease and ways to treat disease are big problems. I was also interested in the history of the disease, unfortunately because of it being such a confined disease, especiialy in the beginning, it was hard to find information on the early stages of the disease. Human African trypanosomiasis (HAT) has been present in Africa since the fourteenth century, it started isolated in pockets due to lack of travel of the indigenous people. The earliest recorded account of sleeping sickness comes from upper Niger and the next report came from Guinea in 1734 (Trypanosoma Brucei – Sleeping Sickness). J. E. Dutton was the first to correctly identify the parasite as a trypanosome and subsequently named it Trypanosoma gambiense in 1902. D. Bruce identified the cause and vector of this disease in 1903, and also the differentiation between the subspecies of the protozoa made in 1910 (Sanger Institute 2011). The first effective treatment, atoxyl, an arsenic-based drug developed by Paul Ehrlich and Kiyoshi Shiga, was introduced in 1910, but blindness was a serious side effect. So next, Suramin was introduced in 1920 to treat the first stage of the disease. By 1922, Suramin was generally combined with Tryparsamide in the treatment of the second stage of the gambiense form. It was used during the grand epidemic in West and Central Africa, helping millions of people, and stayed the mainstay of therapy until 1969 (Medical Ecology). Pentamidine, a highly effective drug for the first stage of the disease, has been used since 1939. During the fifties, it was widely used as a prophylactic agent in Western Africa, leading to a sharp decline in infection rates. At the time, it was thought that eradication of the disease was at hand (Kelly, J. M 2012). This disease has been around for thousands of years, and has been mostly confined to Africa. Of the 36 countries considered endemic for HAT, the seven most affected countries represent 97% of all reported cases. The Democratic Republic of the Congo alone accounts for 2/3 of reported cases. HAT primarily occurs in the poorest, most rural areas in Africa, where difficulty of diagnosis, political instability, and lack of health surveillance make estimates of disease difficult to conduct. It is also a highly focal disease often characterized by distinct outbreaks in a specific area or village (Agriculture and Consumer Protection). Sleeping sickness endemic areas receive their names from geographical features such as rivers, villages or towns, and administrative divisions, and the size of these areas can range from a single populated place to an entire region. Within a given endemic area, the intensity of the disease can vary from one village to the next. Also, the geographical extent of foci may change significantly over time, as a result of both human mobility and of environmental dynamics and modifications influencing tsetse fly presence, density, and dispersal. Furthermore, it was shown that the Rhodesian form of the disease might be introduced into previously unaffected areas by cattle movement. The disease is found all over Africa, and the organism is transferred when bitten by the fly (Odero, R. O 2012). Trypanosoma brucei is the protozoan that causes HAT. There are 3 sub-species of T. brucei: T. b. brucei, T. b. gambiense, and T. b. rhodesiense. T. brucei gambiense causes slow onset chronic trypanosomiasis in humans this is most common in western and central Africa, where humans are thought to be the primary reservoir. T. brucei rhodesiense causes fast onset acute trypanosomiasis in humans, it is most common in eastern and southern Africa, where game animals and livestock are thought to be the main reservoir. Lastly, T. brucei causes animal African trypanosomiasis, along with several other species of trypanosoma. You read "Microbiology Research Paper" in category "Free Research Paper Samples" These are all obligate parasites, parasitic organisms that cannot complete their life cycle without exploiting suitable hosts, which means they live within an insect vector and a mammal host (World Health Organization 2012). The trypanosome goes through complex changes throughout its life due to the large differences between its two hosts. The cell is a fairly typical eukaryotic cell. It features flagella, the cytoskeleton that is made up mostly of microtubules, and the only unusual feature it has is a single, large mitochondria (Van Den Abbeele, Caljon, De Ridder, De Baetselier, Coosemans 2010). African trypanosomes are extracellular organisms, both in the mammalian and insect host. The morphologically is indistinguishable, measuring 25-40  µ m in length. Infection in the human host begins when the infective stage, known as the metacyclic stage, is injected intradermally by the tsetse fly. The organisms rapidly transform into blood-stage trypomastigotes, and divide by binary fission in the interstitial spaces at the site of the bite wound. The buildup of metabolic wastes and cell debris leads to the formation of a chancre. One of its unusual features is that the entire DNA of the mitochondrion, is localized in the kinetoplast, adjacent to the flagellar pocket. Kinetoplast DNA exists in two forms: mini-circles and maxi-circles. Mini-circle DNA encodes guide RNAs that direct extensive editing of RNA transcripts post-transcriptionally. Maxi-circle DNA contains sequences that, when edited, direct translation of typically mitochondrially-encoded proteins. In the vertebrate host, trypanosomes depend entirely upon glucose for energy and are highly aerobic, despite the fact that the kinetoplast-mitochondrion completely lacks cytochromes. Instead, mitochondrial oxygen consumption is based on an alternative oxidase that does not produce ATP. When in the insect vector, the parasite develops a conventional cytochrome chain and TCA cycle. The surface of the trypanosome has numerous membrane-associated transport proteins for obtaining nucleic acid bases, glucose, and other small molecular weight nutrients. None of these proteins react well with antibodies, because although they lie in exposed regions of membrane, they are shielded by allosteric interference provided by the variant surface glycoprotein coat proteins. The number of parasites in the blood is generally so low that diagnosis by microscopic examination is often negative. At some point, trypanosomes enter the central nervous system, with serious pathological consequences for humans. Some parasites transform into the non-dividing short, stumpy form, which has biochemistry similar to those of the long, slender form and the form found in the insect vector (Jackson, Sanders, Berry, McQuillan, Aslett, et al 2010). African Sleeping Sickness is mostly transmitted through the bite of a tsetse fly, but there are also other ways people can be infected. It can be transferred from a mother to child through crossing the placenta and infecting the fetus. Mechanical transmission can happen through other blood-sucking insects, this happens on a much smaller scale than the tsetse fly. Although this number is very small, accidental infections have happened in labs where people are pricked with contaminated needles (Trypanosoma Brucei – Sleeping Sickness). In the first stage, the trypanosomes multiply in subcutaneous tissues, blood and lymph. This is known as a haemolymphatic phase, which entails bouts of fever, headaches, joint pains and itching. In the second stage the parasites cross the blood-brain barrier to infect the central nervous system. This is known as the neurological phase (Kelly 2012). In general this is when more obvious signs and symptoms of the disease appear: changes of behaviour, confusion, sensory disturbances and poor coordination. The symptoms and signs of sleeping sickness are usually quite different, but can be easily confused because of the variability of symptoms and length of time until onset depends heavily on host characteristics. The chancre, a leathery swelling at the site of the bite, is usually the first symptom of the disease, primarily for T. b. rhodensiense. Within weeks, those with opportunistic levels of infection with T. b. rhodensiense start to experience irregular intermittent fevers associated with the waves of parasitaemia that are characteristic of T. b. rhodensiense infections. For T. b. gambiense, lymphoadenopathy occurs more frequently. Oedema of the face is another frequent sign of infection, and anemia may be present, particularly in T. b. rhodensiense (News Medical 2007) Disturbance of the sleep cycle, which gives the disease its name, is an important feature of the second stage of the disease. Since the parasite constantly changes its surface, it can avoid the immune defense of humans and invade the central nervous system, which leads to personality disturbances, sleep disruptions, and ultimately death (Medical Ecology). For patients affected by a severe T brucei infection in the central nervous system, there are no medicines that can treat both subspecies without incurring extremely serious side effects. Although symptoms and signs associated with nervous system involvement are varied for African sleeping sickness, advanced disease epileptic seizures, maniacal behavior, somnolence, and coma are some typical late stage symptoms (African Trypanosomiasis [also known as Sleeping Sickness] 2010). Unfortunately, survival rates are drastically reduced once the trypanosomes infect the central nervous system. The disease management is made up of three steps: the first is the screening for potential infection by serological tests and checking for clinical symptoms. The second step is to diagnose whether the parasite is present in the body or not, and the final step is to determine the progression of the disease, usually by examining cerebro-spinal fluid. Today, there are only a handful of active drugs available for treatment of human African Trypanosomiasis, and no significant development has been made over the last 2 decades. The current line of treatment is problematic for many reasons: firstly, the drugs are harmfully toxic requiring extensive hospitalization. Secondly, regular follow-ups to check for relapse is essential but difficult in many of the areas where sleeping sickness is endemic (News Medical 2007). Many individuals die before they can ever be treated for the disease because the first stage is usually asymptomatic, and in Africa, an extensive testing of a large number of people who may or may not be infected, is to costly of an investment. The type of treatment depends on the progression of the disease. As it is in most diseases the earlier it is identified, the easier it is to treat and cure. The drugs used in the first stage of the disease are of lower toxicity and easier to administer. Treatment success in the second stage depends on a drug that can cross the blood-brain barrier to reach the parasite. Such drugs are toxic and complicated to administer (African Trypanosomiasis [also known as Sleeping Sickness] 2010). Over the past years, public awareness of the dangers associated with insecticides is increasingly changing the way we treat our environment. Efforts to introduce more environmentally friendly methods of insect control provide the world with challenges to understand more about the insects that transmit HAP. We live in a modern world where various means of control are available to stop the spreading of multiple diseases, however, sleeping sickness is a disease of the developing world. In Africa, despite the multitude of control strategies, issues have been widely neglected and abandoned. One of the main components needed to bring effective change, is to consider a control strategy that will last and can be carried through by local communities (Jackson, Sanders, Berry, McQuillan, Aslett, et al 2010). Apart from efforts to reduce the spread of disease through environmental controls, there is also need to improve current tracking and diagnostic procedures. Chances of death can be drastically reduced when cases can be diagnosed early enough to prevent onset of late-stage sleeping sickness. Training and resources are desperately needed in affected areas for safe and proper diagnostics. With this disease there is an issue with treatment options, and the availability of drugs in Africa. Drug and vaccine development for diseases in developing countries have always been lagging, and trypanocidal drugs are no exception. An estimated 300,000 to 500,000 people are currently infected and suffering from HAT with no hope for treatment. In 2000, the USFDA approved the use of eflornithine. Hopefully some of the profits from the sale of this drug are used to help the situation in the poorest parts of Africa infected with this disease (Jackson, Sanders, Berry, McQuillan, Aslett, et al 2010). The biggest issue with this disease is that it is confined to people in Africa. Because of this most of the world is not aware of the seriousness of it, and most people do not know how they can help. Also, with all the diseases in Africa, many smaller scale sicknesses can be overlooked. Third world countries often have trouble being able to control all the different infections that affect so many people in them. Researching this opened my eyes to the multiplicity and severity of the diseases that affect so many people. It was shocking to learn that this disease has been around for a few thousand years and people are still dying of it daily. And furthermore, that this was the first time I had ever even heard of the disease. It was really interesting to learn about the tsetse fly also, the only other sickness I had heard of before that was transferred by a blood sucking insect, was malaria. The hardest thing to understand was how although there is a cure for this disease, people are still dying of it every day. I was not aware of the complete lack of technology and awareness of the illness in the places affected. If I were to research further on HAT, I would like to research about foundations that donate and help the people and countries affected by this disease. I am very interested in charities and companies that help the less fortunate. Overall, the research I did on this subject has been very informative and thought provoking, it has made me a more knowledgeable person on not only this specific disease, but also many diseases killing people in Africa and other third world countries. I learned a lot about the aspects of microbiology, I got to see it applied to the real world and the affects it can have on people. This has better informed me about the course I am taking and the application of it to something other than a lab station. I learned so much more than I needed to know, but it has made me a better person in the long run, I am a better, smarter person after writing this paper. How to cite Microbiology Research Paper, Essays Microbiology Research Paper Free Essays string(98) " to nonciliated epithelial cells through pili and the production of lipopolysaccharide endotoxin\." Melissa Babajko Microbiology 214BA Dr. May June 6, 2012 Staphylococcus aureus- Is a facultative anaerobic, Gram-positive, salt positive, cocci shaped bacterium. Staphylococcus aureus is found as normal part of the skin floral in the nasal passages and on the skin. We will write a custom essay sample on Microbiology Research Paper or any similar topic only for you Order Now An estimated twenty percent of people naturally have harmless Staphylococcus aureus on their skin and are long-term carries for Staphylococcus aureus. Staphylococcus aureus is the most common strand of Staphylococcus in humans to date, spread through skin to skin contact or even skin to object contact that an a person infected with Staphylococcus aureus has touched. Staphylococcus aureus is coagulase positive, which induces clumping of the cells and of the blood. Staphylococcus aureus has many immune-evasive strategies that make it the most common strand, such as; it produces leukocidin a toxin that kills white blood cells. It also resists opsonization, survives in phagolysosomes, and is lysozyme resistant. Methicillin-resistant S. aureus, abbreviated MRSA, is one of a number of greatly feared strains of S. aureus, which have become resistant to most antibiotics. MRSA strains are most often found associated with institutions such as hospitals, but are becoming increasingly prevalent in community-acquired infections. Research Study: IBM, the computer company, working on nanoparticles that polymerize into structures that are able to attack MRSA bacteria without harming the healthy tissue around it. Once these polymers come into contact with water in or on the body, they self assemble into a new polymer structure that is designed to target bacteria membranes based on electrostatic interaction and break through their cell membranes and walls. The physical nature of this action prevents bacteria from developing resistance to these nanoparticles or other antibiotics. The electric charge naturally found in cells is important because the new polymer structures are attracted only to the infected areas while preserving the healthy red blood cells the body needs to transport oxygen throughout the body and combat bacteria. Unlike most antimicrobial materials, these are biodegradable, which enhances their potential application because they are naturally eliminated from the body (rather than remaining behind and accumulating in organs). They are calling this â€Å"nanomedicine† and if the trial tests work this could destroy this superbug and eliminate MRSA from hotspots like hospitals. (http://www. forbes. com/sites/amywestervelt/2012/05/16/how-ibm-plans-to-solve-the-mrsa-problem/) Streptococcus pyogenes- Is a gram- positive, spherical, group a, beta-hemolytic bacterium. Streptococcus pyogenes displays Streptococcus antigen A in its cell wall surface. Streptococcus pyogenes has M-protein on its surface, which are fibrils that are antiphagocytic and are involved in the adherence to the skin and mucos membranes. Streptococcus pyogenes is a catalase negative bacterium that has a capsule that prevents the bacterium from phagocytosis and neutrophils. Another immune-evasive property of Streptococcus pyogenes is the M-proteins on its surface inhibit opsonization. Streptococcus pyogenes is the cause of many human diseases ranging in severity. Disease in a result to infection includes, pharyngitis (sore throat), impetigo and invasive infections such as, cellulitis and erysipelas. Research Study: Portuguese scientists are looking at new ways to combat the spread of Streptococcus pyogenes by looking into natural antimicrobials. This work aimed to screen the antimicrobial activity of aqueous methanolic extracts of 13 mushroom species. Scientist used a microdilution method to determine the Minimum Inhibitory Concentration (MIC) and the Minimum Bactericidal Concentration (MBC). MIC results showed that Russula delica and Fistulina hepatica extracts inhibited the growth of Streptococcus pyogenes. A MBC of 10 mg/ml of Ramaria botrytis extract shoed to have bactericide effects on Streptococcus pyogenes, leading scientist to conclude that mushroom extracts could be a hopeful species as an antimicrobial agent to Streptococcus pyogenes that may be resistant to traditional treatments. (http://www. ncbi. nlm. nih. gov/pubmed/22621239) PMID: 22621239 [PubMed – as supplied by publisher] May 2012 Streptococcus pneumoniae- Is a Gram-positive bacterium in the shape of a slightly pointed cocci. They are usually found in pairs as diplococci. Streptococcus pneumoniae are alpha hemolytic bacterium. Streptococcus pneumoniae have a polysaccharide capsule that acts as a virulence factor for the organism; along with surface proteins that prevent the activation of complement pathways, and pili that enable S. pneumoniae to attach to epithelial cells in the upper respiratory tract. Streptococcus pneumoniae lacks catalase and ferments glucose to lactic acid, like most other streptococci. However, unlike most other streptococci, it does not display an M protein and it hydrolyzes insulin, which help distinguish it from other streptococci. Streptococcus pneumoniae is the most common cause of meningitis in adults and young adults throughout the world and is best known for causing pneumonia all other the world. Research Study: Due to a continuing increase in S. pneumoniae’s antibiotic resistance, the search for a better vaccine is ongoing. Research on the Lactococcus lactis bacteria for use as a vaccine is promising; its production of the pneumococcal surface protein PspA makes it a good candidate for a mucosal vaccine, which could be administered through the nose instead of an injection (a promising aspect). Studies show that the lactococcal vaccine offers better protection against respiratory infection by S. pneumoniae than injections of similar amounts of recombinant PspA administered by injection. There is considerable potential to develop a vaccine with L. lactis, for use against S. streptococcus and more. (http://www. journals. uchicago. edu/JID/journal/issues/v195n2/36706/brief/36706. abstract. html? erFrom=-2043069302250900887Guest) Neisseria gonorrhoeae- Is a gram-negative cocci that are shaped like coffee beans and grow as diplococcic. Neisseria gonorrhoeae grow on chocolate agar with carbon dioxide and need nutrients to grow in a laboratory setting. Neisseria gonorrhoeae are motile bacterium, which move around by twitching and have type IV pilli to adhere to surfaces. Neisseria gonorrhoeae is able to prevent an immune response by using its surface opa proteins, which bind to receptors on immune cells. This results in the host being unable to develop an immunological memory against Neisseria gonorrhoeae and allow for the possibility of reinfection. Neisseria gonorrhoeae infections are acquired by sexual contact and usually affect the mucous membranes of the urethra in males and the endocervix and urethra in females. The pathogenic mechanism involves the attachment of the bacterium to nonciliated epithelial cells through pili and the production of lipopolysaccharide endotoxin. You read "Microbiology Research Paper" in category "Essay examples" Neisseria gonorrhoeae is only found after sexual contact with an infected person (or in the case of infections in the newborn, direct contact). Research Study- A single dose of cefodizime (CDZM), ceftriaxone(CTRX), or spectinomycin (SPCM) is what is recommended for the treatment of gonococcal urethritis or uterine cervicitis. It was previously found that a single dose of CDZM completely eradicated multidrug-resistant N. gonorrhoeae in patients with urethritis and uterine cervicitis, and so a single 1. 0-g dose of CDZM for the treatment of N. gonorrhoeae pharyngeal infection, including infections with CZRNG was tried. The eradication rate of N. gonorrhoeae from the pharynx was 63. % with a single 1. 0-g dose of CDZM, while the rate for CZRNG with the same dose of CDZM was 38. 5%. N. gonorrhoeae was completely eradicated from the pharynx when patients received one or two additional doses of CDZM. It was found that N. gonorrhoeae was completely eradicated from the pharynx when patients received one or two additional doses of CDZM. Therefore, it can be concluded that two to three doses of CDZM are necessary for the treatment of CZRNG pharyngeal infection. (http://www. ncbi. nlm. nih. gov/pmc/articles/PMC1636252/) Escherichia coli- Is an aerobic, gram-negative, rod shaped bacteria that can be commonly found in animal feces and in the lower intestines of mammals. Escherichia coli possesses adhesive fimbriae and a cell wall that consists of an outer membrane containing lipopolysaccharides, a periplasmic space with a peptidoglycan layer, and an inner, cytoplasmic membrane. The lipopolysaccharide layer of Escherichia coli contains an endotoxin called lipid A and also have a capsule that help fight against phagocytosis and add to its virulence. Some strains are piliated and capable of accepting and transferring plasmid to and from other bacteria. Escherichia coli prefer to live at a higher temperature rather than the cooler temperatures. The harmless strains of Escherichia coli are part of the normal flora in the gut and benefit the host organism by producing vitamin K and preventing the development of pathogenic bacteria within the intestine. Although Escherichia coli is harmless in the gut of an organism when it enters the blood stream and travels through the body it then becomes the leading cause for food poisoning among humans and when it enters the urethra it can cause urinary tract infections in both males and females. Research Study- A study is focusing on exploring the antigens on the outer membrane of the uropathogenic E. coli (UPEC) which can cause uncomplicated urinary tract infection (UTI), and furthermore to design a UTI vaccine to promote protective immunity against UPEC infection. In this sutdy, they apply an immunoproteomics approach to vaccine development that has been used successfully to identify vaccine targets in other pathogenic bacteria. The outer membrane proteins of UPEC from infected mice are separated by two-dimensional gel electrophoresis and are identified by mass spectrometry. A total of 23 antigens have known roles in UPEC pathogenesis, such as ChuA, IroN, IreA, Iha, IutA, and FliC. After identifying the antigens on outer membrane of UPEC, they demonstrate an antibody targeting directly on these antigens during UTI. This study shows that these conserved outer membrane antigens can be used as rational candidates for a UTI vaccine. (http://www. ncbi. nlm. nih. gov/sites/entrez? Db=pubmed;Cmd=ShowDetailView;TermToSearch=17525800;ordinalpos=7;itool=EntrezSystem2. PEntrez. Pubmed. Pubmed_ResultsPanel. Pubmed_RVDocSum) Haemophilus influenzae- Is a gram-negative bacterium, which infects the blood stream of the organism, which is shaped like rods and is generally anaerobic in nature but can live as facultative anaerobic. Haemophilus influenzae was discovered around the flu pandemic and was first thought to be the cause of influenza but was disproven shown to be the cause of many other clinical diseases. Haemophilus influenzae has new strands of bacterium that can affect organism there is an unencapsulated strain and an encapsulated strain, which is the most common strain to infect humans. Haemophilus influenzae lack motility due to their lack of flagella and pilli, the capsulated strains have a polysaccharide capsule which has the endotoxin Lipid A that contributes to Haemophilus influenzae ability to survive in the blood stream. H. influenzae is an opportunistic pathogen that normally lives with in the host without causing any problems but will act on an opportunity such as a compromised immune system to infect the host. The most noted strain; H. influenzae type b causes meningitis, which is an inflection in the membrane around the brain and epiglottitis, which is infection around the throat and trachea. In general H. Influenzae bacteria lives in the upper respiratory tract, which can be transmitted by close contact with patients. This bacterial infection can also be air born transmitted through sneezing. Research Study- Arnold Smith, M. D. from Seattle Biomedical Research institute, has preformed a research study on how h. influenzae operates. In this research, Dr. Smith’s purpose is to understand how this bacterium causes disease, which can help improved current treatments and preventions. In the lab molecular mechanisms of h. nfluenzae was understood. It was also noted that specific strains of this bacteria have ability to cross the respiratory tract of young children. It was also found that once this infection enters the blood stream it might cause sepsis and meningitis. This research is currently in progress at the Seattle Biomedical Research Institute. (http://www. sbri. org/research/a_smith. asp) Clostridium tetani- is a bacillus, or rod-shaped, bacterium. It is Gram po sitive and commonly appears to be shaped like a drumstick or tennis racket when stained. This appearance is due to the sporulation that occurs inside the cell. Clostridium tetani is an obligate anaerobe and relies on fermentation to survive. Clostridium tetani possess a thick cell wall made up of multiple layers of peptidoglycan and one inner membrane. C. tetani are motile bacteria and move with the use of their of rotary flagellum. C. tetani in the presence of oxygen changes into its endospore form, the spores of Clostridium tetani are resistant to resistant to heat and some antiseptics which contribute to its ability to spread and infect organisms. Clostridium tetani affects humans by causing the disease tetanus. Clostridium tetani enters the body through an open wound where its spores can use the environment created by the dead cells to start its anaerobic processes. The spores begin to produce the toxin tetanospasmin, which travels throughout the body via the nervous system. Once tetanospasmin reaches the spinal cord where it begins to interfere with neurotransmitters which blocks messages to the brain this leads to unwanted muscle contractions and spasms, and individuals can experience severe seizures. Research Study- A 2008 study in Kano, Nigeria sought to determine the susceptibility of Clostridium tetani to various antibiotics. Soil was collected from five different locations and cultured under anaerobic conditions to observe the number of samples, which contained Clostridium tetani spores. The bacterium was observed in 60% of the soil samples. The samples were treated with amoxicillin, chloramphenicol, tetracycline, erythromycin, augmentin, co–trimoxazole, metronidazol, penicillin V, gentamycin, cloxacillin, sparfloxacin and ciprofloxacin to determine antibiotic susceptibility. The most effective antibiotic in preventing colony growth was observed to be sparfloxacin, with erythromycin, tetracycline, gentamycin, chloramphenicol, metronidazole and ciprofloxacin also preventing growth. The remaining antibiotics appeared to be inaffective against Clostridium tetani. (http://www. ajol. info/index. php/bajopas/article/viewFile/57539/45918) Mycobacterium tuberculosis- Is a acid fast bacterium that is rod shaped that usually form in clumps and are obligate aerobe. Mycobacterium tuberculosis has a cell envelope that contains a polypeptide layer, a peptidoglycan layer, and free lipids. In addition, there is also a complex structure of fatty acids such as mycolic acids that appear glossy. These lipids are resoponsible for the mycobacterium survival under environmental stressors. Mycobacterium tuberculosis utilizes its cell envelope to prevent it from drying out and allows it to survive weeks in dried septum also it makes Mycobacterium tuberculosis resistant to chemical antimicrobials. Mycobacterium tuberculosis reaches the lungs of a human by inhalation of bacillus, in the lungs, M. tuberculosis is taken up by alveolar macrophages, but they are unable to digest the bacterium. Its cell wall prevents the fusion of the phagosome with a lysosome allowing the bacterium to replicate with in the macrophage letting the disease spread. Mycobacterium tuberculosis causes the respiratory disease tuberculosis, which leaves a person infectious to spread the disease through the air, person to person, by the cough that they have devolped from the disease. Tuberculosis can infect anyone but is more common in immunosuppressed patients and if left untreated can be deadly. Vaccinating individuals with the BCG vaccine to stop the spread of this growing global epidemic is doing prevention of the spread of tuberculosis. Research Study- A group of scientists found that a newly identified protein with carboxyesterase activity is required for the virulence of Mycobacterium tuberculosis. They found that the gene MT2282 encodes a protein that is associated with carboxyesterase. It hydrolyzes ester bonds of the substrate. When a strain containing a mutant of this gene was used to infect mice, the mice’s life was prolonged as compared with those that were infected with the wild type strain. (â€Å"Characterization of a novel cell wall-anchored protein with carboyesterase activity required for virulence in Mycobacterium tuberculosis. The Journal of Biological Chemistry 2007) Treponema pallidum- is a Gram-negative bacterium, which is spiral in shape. It is an obligate internal parasite, which causes syphilis, a chronic human disease. Syphilis is a sexually transmitted disease but transmission can also occur between mother and child in utero; this is called congenital syphilis. Syphilis was first disc overed in Europe near the end of the fifteenth century. Treponema pallidum is an obligate internal parasite, meaning that it requires a mammalian host for survival. In the absence of mammalian cells, T. allidum will be killed by the absence of nutrients, exposure to oxygen and heat. T. pallidum lacks enzymes necessary to build complex molecules and loses its infectiousness when outside the host mammal for too long. T. pallidum has slim to none virulence factors but it produces several lipoproteins that induce and inflammatory response from the immune system resulting in the tissue destruction that goes along with this disease. Once T. pallidum infects the host it immediately enters the bloodstream and moves through deeper tissue with ease because of their corkscrew-like motility. Untreated syphilis progresses in a series of distinct stages. Primary syphilis usually presents itself as a single chancre at the site of infection. Secondary syphilis occurs approximately 3 months after infection and presents itself as lesions of the skin and mucous membranes. These include a rash commonly on the palms of the hands, soles of the feet, face, and scalp. The breakdown of mucous membranes appears as patches on lips, inside the mouth, vulva, and vagina. If untreated it may progress to tertiary phase. Tertiary syphilis can cause destructive lesions on skin and bones, which are usually benign. The more deadly manifestations of late syphilis affect the cardiovascular system and the central nervous system causing infected individuals to experience insomnia and changes in personality. If detected early syphilis is easily eradicated from the host by benzathine penicillin. Research Study- The current method for detecting syphilis is based on recognition of its signs and symptoms followed by blood tests which lack sensitivity and require fresh serum. The goal of this study was to develop a sensitive assay to directly test for syphilis. They were able to develop a TaqMan real-time PCR assay that was able to detect T. pallidum from â€Å"swabs and biopsy specimens from genital and mucosal ulcers, placental specimens, and cerebrospinal fluid. â€Å" Further research is required to confirm the accuracy of this new assay. This will be done by comparing results of this new method against other currently used test for syphilis. (:http://www. pubmedcentral. nih. gov/articlerender. fcgi? tool=pubmed;pubmedid=17065262) Chlamydia trachomatis- Is an obligate, aerobic, intracellular parasite of eukaryotic cells. It is a Gram-negative bacterium and has a coccoid or rod shape. It has a cytoplasmic membrane and outer membrane similar to Gram-negative bacteria but lacks a peptidoglycan cell wall. C. trachomatis require growing cells in order to remain viable since it cannot synthesize its own ATP. Without a host organism, Chlamydia trachomatis cannot survive on its own. C. trachomatis is the leading cause of sexually transmitted disease worldwide–in the United States, alone, over 4 million cases are diagnosed each year. It is also the leading cause of preventable blindness in the world. Chlamydia trachomatis is also one of the major causes of pelvic inflammatory disease (PID) and infertility in women. Chlamydia is transmitted through infected secretions only. Usually, Chlamydia trachomatis is asymptomatic in its hosts, but can cause discharge from the penis, pain and burning during urination, infection or inflammation in the ducts of testicles, and tenderness or pain in the testicles. It infects mainly mucosal membranes, such as the cervix, rectum, urethra, throat, and conjunctiva. It is primarily spread via sexual contact and manifests as the sexually transmitted disease. The bacterium is not easily spread among women, so the STD is mainly transmitted by heterosexual or male homosexual contact. However, infected secretions from the genitals to the hands and eventually to the eyes can cause trachoma. There is no vaccine to stop the spread of Chlamydia but the disease can be cured very eaily with antibiotics. Research Study- Current research uses a live-attenuated form of the influenza A virus to provide viral vector for a vaccine against C. trachomatis. This vaccine is tested to be used intra-nasally. In the experiment, mice were intra-nasally immunized with influenza A viral recombinants. The result was a very strong immune, T helper 1, response against intact Chlamydia trachomatis elementary bodies. The genital secretions in the mice showed high levels of specific Th1 cells and elevated immunoglobulin G2a, which indicates a possibility of long term, protective immunity. This study, using C. trachomatis, is very important because it indicates that live attenuated vaccines of the influenza virus could be a new and reliable approach to preventing the spread of sexually transmitted disease. (http://www. ncbi. nlm. nih. gov/sites/entrez? Db=pubmed;Cmd=ShowDetailView;TermToSearch=17451464) Herpes simplex virus I and II- are two members of the herpes virus family, Herpesviridae, that infect humans. The structure of herpes viruses consists of a relatively large double-stranded, linear DNA genome encased within an icosahedral protein cage called the capsid, which is wrapped in a lipid bilayer called the envelope. The envelope is joined to the capsid by means of a tegument. This complete particle is known as the virion. A herpesvirus infection begins with attachment to and penetration of a host cell. Since herpesviruses are large DNA viruses, and they usually infect non-dividing cells, they encode enzymes involved in nucleic acid metabolism and DNA synthesis so they can copy their DNA once they enter the host cell. Herpesviruses replicate in the nucleus of the host cell. HSV-1 is the cause of oral herpes producing what are commonly known as cold sores. HSV-2 is the cause of genital herpes crating lesions and blisters on the genitals of the infected organism. Ss neurotropic and neuroinvasive viruses, HSV-1 and -2 persist in the body by becoming latent and hiding from the immune system in the cell bodies of neurons. After the initial or primary infection, some infected people experience sporadic episodes of viral reactivation or outbreaks. In an outbreak, the virus in a nerve cell becomes active and is transported via the neuron’s axon to the skin, where virus replication and shedding occur and cause new sores. HSV-1 and -2 can both be treated but never cured and rid from the body. Research Study- In this study, researchers applied an experimental feedback system control (FSC) method and rapidly identified optimal drug combinations that inhibit herpes simplex virus-1 infection, by only testing less than 0. % of the total possible drug combinations. Using antiviral efficacy as the criterion, FSC quickly identified a highly efficacious drug cocktail. This cocktail contained high dose ribavirin. Ribavirin, while being an effective antiviral drug, often induces toxic side effects that are not desirable in a therapeutic drug combination. To screen for less toxic drug combinations, we applied a second FSC search in cascade and used both high antiviral efficacy and low toxicity as criteria. Surprisingly, the new drug combination eliminated the need for ribavirin, but still blocked viral infection in nearly 100% of cases. This cascade search provides a versatile platform for rapid discovery of new drug combinations that satisfy multiple criteria. (http://www. ncbi. nlm. nih. gov/pubmed/22654513) Epstein-Barr virus- Epstein Barr Virus (human herpesvirus 4 or EBV) is a member of the herpesvirdidae family. Epstein Barr Virus is the most common and most successful human virus. Epstein Barr Virus occurs worldwide, affecting anyone at any point in his or her lifetime, selectively infecting B-lymphocytes. Once infected the virus stays with the person for the rest of their life, remains latent in B cells after recovery from the disease. The structure of Epstein-Barr virus is a icosahedral nucleocapsid. The nucleocapsid is composed of 162 capsomers. The nucleocapsid is then surrounded by a protein outer covering, which is then surrounded by a viral envelope that contains numerous glycoproteins. EBV only infects humans. Replication of Epstein Barr Virus can occur in two ways: Infection of skin cells that results in lysis of host cells and release of virions. ; primary B-cell that results in latency infection. During this stage the virus is constantly being repilicated. The most common condition that EBV is associated with is infectious mononucleosis, which is transmitted via saliva and is characterized by proliferation of lymphocytes. The symptoms of infectious mononucleosis are fever, fatigue, sore throat, tonsillitis, adenopathy and hetatomegaly. The virus causes disease either by lysis of host cells to release virions or by continuous replication during the latency cycle. Research Study- Vaccine production- scientists are researchers are trying to create a vaccine for prevention of Epstein Barr Virus. The problem is with all the diseases that are caused by EBV, would be difficult to cure these diseases. Also most people with EBV don’t even know they have it and if there aren’t any clincial symptoms reported, researchers cannot create a vaccine. (2007. Pathogenesis and Therapy of Epstein-Barr Virus Infection: Novel Therapeutic Approaches. 1-37. In: New Developments in Epstein-Barr Virus Research. ) Hepatitis C virus- The virions of Hepatitis C virus are spherical and consist of an envelope and a nucleocapsid, a detergent sensitive lipoprotein envelops the virus capsid. The genome of hepatitis C virus is not segmented and contains a single molecule of linear positive-sense, single stranded RNA. Hepatitis C virus is spread by blood-to-blood contact, through unsterilized medical equipment, healthcare exposure, sexual intercourse, and drug use, its as only existent in humans and chimpanzees. The disease primarily affects the liver but often shows no sign of infection. When this viral disease reaches the chronic stage it leads to inflammation of the liver leading to the formation of scar tissue and cirrhosis. Cirrhosis can lead to liver failure or cancer and may result in the infected needing a liver transport. There is no vaccine currently available for the Hepatitis C virus. Research Study- Researchers conducting a open-label, phase 2a study included an exploratory cohort of 21 patients with chronic HCV genotype 1 infection who had not had a response to previous therapy. Researchers randomly assigned patients to receive the NS5A replication complex inhibitor daclatasvir (60 mg once daily) and the NS3 protease inhibitor asunaprevir (600 mg twice daily) alone (group A, 11 patients) or in combination with peginterferon alfa-2a and ribavirin (group B, 10 patients) for 24 weeks. The primary end point was the percentage of patients with a sustained virologic response 12 weeks after the end of the treatment period. This preliminary study involving patients with HCV genotype 1 infection who had not had a response to prior therapy showed that a sustained virologic response can be achieved with two direct-acting antiviral agents only. In addition, a high rate of sustained virologic response was achieved when the two direct-acting antiviral agents were combined with peginterferon alfa-2a and ribavirin. (http://www. ncbi. nlm. nih. ov/pubmed/22256805) Hepatitis B virus- The virion consists of an outer lipid envelope and an icosahedral nucleocapsid core composed of protein. These virions are sometimes referred to as â€Å"Dane particles†. The nucleocapsid encloses the viral DNA and a DNA polymerase that has reverse transcriptase activity. The outer envelope contains embedded proteins that are involved in viral binding of, and entry into, susceptible cells. He patitis B virus is one of the smallest enveloped animal viruses. The protein of the virion coat is known as â€Å"surface antigen† or HBsAg. Hepatitis B virus is only found in humans and chimpanzees and was originally known as the serum virus. The virus is transmitted by exposure to infectious blood or body fluids such as semen and vaginal fluids. The acute illness causes liver inflammation, vomiting, jaundice and, rarely, death. Chronic hepatitis B may eventually cause cirrhosis and liver cancer but this disease responds poorly to treatment. Hepatitis B virus is currently preventable by vaccination. Research study- One thousand twenty pregnant women and 946 patients visiting for routine checkups were screened for HBV and HDV infection. Demographic, epidemiological, ethnic, clinical, and biological data were recorded. In pregnant women, exposure to HBV was significantly associated in multivariate analysis with education level, ethnicity, blood transfusion, and occupation. HDV antibodies (HDVAb) were found in 14. 7% of pregnant women. In patients, HBsAg was found less frequently in females than in males. Again in multivariate analysis, exposure to HBV was significantly correlated with gender (males), and HDVAb positivity with age and gender. This study confirms the high prevalence of HBV and HDV infections in Mauritania and demonstrates the high genetic diversity of HBV in this country. (http://www. ncbi. nlm. nih. gov/pubmed/22711346) Influenza A virus- Is more commonly known as bird flu or avian influenza. Influenza A virus is part of the Orthomyxoviridae group. Influenza A viruses are negative sense, single-stranded, segmented RNA viruses. There are two different classifications of Influenza A virus, highly pathogenic avian influenza (HPIA) and mildly or non-pathogenic avian influenza (MPIA). The virus has a protein envelope encasing it. There are different variations of Influenza A virus based on their H number (for the type of hemagglutinin) and an N number (for the type of neuraminidase), which gives it the name H1N5. Wild birds are the natural host for all known subtypes of Influenza A viruses but it is known to infect domestic birds as well becoming a natural killer for them and also passing this disease, although rare, onto humans. There is currently a Influenza A virus vaccine developed to help stop the spread of an Influenza A virus epidemic if one were to ever occur. Research Study- Researches debate on a global scale, about bioethics, biohazard, bio weaponry and bioterrorism issues related to scientific research concerning the induced transition of the highly lethal H5N1 avian flu virus from a non-pandemic to a tentatively pandemic strain, which might fall into malevolent hands. Appreciable ecogenetic complexity marks the main attributes of influenza type A viruses, namely infectivity, virulence, antigenicity, transmissibility, host range, endemicity, and epidemicity. They all shape, conjunctively, the outstanding protean nature of this pathogen, hence the modularity of the latter as a potent weapon. Altogether, a variety of interrelated properties underlying the complicatedness of and menaces posed by influenza A virus as a grave medical challenge, a dually explorable pathogen, and a modular biological warfare agent, are thereby illuminated, alongside with their scientific, strategic and practical implications. (http://www. ncbi. nlm. nih. gov/pubmed/22690739) Human immunodeficiency virus- Is a positive-sense single stranded RNA virus that belongs to the genus Lentivirus and the family Reteroviridae. The virions of an HIV consist of an envelope, a nucleocapsid, a nucleoid, and a matrix protein. The virus capsid is enveloped. The virions are spherical to pleomorphic with small but high numbers of surface projections that are called glycoprotein spikes that allow the virus to dock to amplifier cells slowing down immune system response. The replication of HIV can only take place inside human cells. The process typically begins when a virus particle bumps into a cell that carries a special protein called CD4 on its surface. The spikes on the surface of the virusparticle stick to the CD4 to allow the viral envelope to fuse with the cell membrane. HIV particle contents are then released into the cell, leaving the envelope behind. The HIV enzyme reverse transcriptase converts the viral RNA into DNA, which is compatible to human genetic material, when the virus is inside the cell. This DNA is transported to the cell’s nucleus, where it is spliced into human DNA by the HIV enzyme integrase. The HIV DNA is known as provirus after it is integrated. HIV takes over the body by attacking CD4 helper T cells lowering its levels leaving the body unable to create a proper immune response and leaving it susceptible to infection. Human immunodeficiency virus has three stages in its infectious process before full-blown Acquired Immunodeficiency Syndrome is in motion. Human immunodeficiency virus has a short life surviving just 6 hours outside the cell and 1 and ? days inside the cell. Sexual contact, breast milk, transplants, and blood-to-blood contact transmit human immunodeficiency virus. Human immunodeficiency virus is the causative agent of Acquired Immunodeficiency Syndrome (AIDS), which leads to many other opportunistic infections, leading most people to die from the new infections rather then AIDS or HIV itself. There is currently no vaccine or treatment for Human immunodeficiency virus but with proper precautionary measures you can control the spread of the virus. Research Study- Researches have discovered that SAMHD1 restricts the infection of dendritic and other myeloid cells by human immunodeficiency virus type 1 (HIV-1), but in lentiviruses of the simian immunodeficiency virus of sooty mangabey (SIVsm)-HIV-2 lineage, SAMHD1 is counteracted by the virion-packaged accessory protein Vpx. Here we found that SAMHD1 restricted infection by hydrolyzing intracellular deoxynucleoside triphosphates (dNTPs), lowering their concentrations to below those required for the synthesis of the viral DNA by reverse transcriptase (RT). SAMHD1-mediated restriction was alleviated by the addition of exogenous deoxynucleosides. An HIV-1 with a mutant RT with low affinity for dNTPs was particularly sensitive to SAMHD1-mediated restriction. Vpx prevented the SAMHD1-mediated decrease in dNTP concentration and induced the degradation of human and rhesus macaque SAMHD1 but had no effect on mouse SAMHD1. Nucleotide-pool depletion could be a general mechanism for protecting cells from infectious agents that replicate through a DNA intermediate. (http://www. ncbi. nlm. nih. gov/pubmed/22327569) Trichomonas vaginalis- Is a parasitic, flagellated protozoan anaerobe. The appearance of this protozoan is altered by physiochemical conditions. In a pure culture, the shape is more uniform such as pear-shaped or oval. As a parasite, it appears more amoeboid when attached to the vaginal epithelial cells. It has five flagella—four of which are in the anterior and the other flagellum is incorporated within the undulating membrane. The flagella and the undulating membrane contribute to its motility. The cytoskeleton is made of tubulin and actin fibers. The nucleus, surrounded by a porous nuclear envelope, is located at its anterior end. A thin hyaline, rod-like structure called the axostyle begins at the nucleus and bisects the protozoan longitudinally. It protrudes through the posterior portion of the protozoan, ending in a sharp point. The axostyle helps anchor the protozoan to the vaginal epithelial cells. Trichomonas vaginalis causes Trichomoniasis which is the most prevalent non-viral sexually transmitted disease. Trichomoniasis is more common in women than men because men have asymptomatic infections. For women, the symptoms are thin frothy, green-yellow vaginal discharge; vulvovaginal irritation, vaginal soreness, and redness of the vagina. Women also have a higher prevalence of invasive cervical cancer when they have trichomoniasis. During pregnancy, there is an increased risk of preterm and low weight babies. Men have non-gonoccocal urethritis and chronic prostatitis. This infection has been found to be associated with prostate cancer. In both sexes, there is a higher susceptibility to HIV and infertility. There are no vaccines avaliabe for to decrease the spread of Trichomonas vaginalis but Trichomoniasis is a curable disease with antibiotics. Research Study- Besides being transmitted sexually, there have been cases of nonsexual transmission of trichomoniasis such as contaminated douche nozzles, specula, toilet seats, or swimming pool water. The role of public swimming pools in spreading the disease is controversial yet there is little research done. The viability of T. vaginalis in samples of water was reexamined by Pereira-Neves and Benchimol. They concluded that T. vaginalis remains viable and infective in swimming pool water samples for several hours. The survival time is dependent on the cytotoxicity of the strain. The possible transmission of trichomoniasis in public swimming pools may be low. (http://www. mendeley. com/research/trichomonas-vaginalis-vitro-survival-swimming-pool-water-samples/) Plasmodium species- Is a parasite that forms sporozites and is the cause for human malaria. There are four types of Plasmodium that cause human malaria: Plasmodium falciparum, Plasmodium ovale, Plasmodium vivax, and Plasmodium malariae. The sporozoites have a thin outer membrane, a double inner membrane below which lies the subpelicular microtubules. They have 3 polar rings and the rhoptries are long, extending half the length of the body. The micronemes, convoluted elongate bodies, run forward to the anterior of the sporozoite entering a common duct with the rhoptries. After entering the circulatory system, the sporozoites make quick work of invading liver cells using the apical organelles inside the host’s liver cell the Plasmodium cell undergoes asexual replication. The products of this replication, called merozoites, are released into the circulatory system. The merozoites invade erythrocites and become enlarged ring-shaped trophozoites. In this stage the cells ingest the host cytoplasm and proteolyze hemoglobin into amino acids. Plasmodium species infect humans by an infected Anophele mosquito bites a human and the sporozoites of a Plasmodium species are injected into the blood with the saliva causing malaria. Malaria symptoms may go unnoticed or misdiagnosed; clinical signs include fever, chills, weakness, headache, vomiting, diarrhea, anemia, pulmonary and renal dysfunction, neurologic changes and untreated malaria may result in death. To prevent the spread of malaria precautions are being taken to monitor the dsease with in the mosquito population and measure and taken to reduce it. Research Study- Incidence rates and vulnerability to malaria are linked to low socioeconomic status. Areas with concentrated populations of people with low socioeconomic status typically do not have resources for effective prevention and subsequent treatment. For example, a study conducted by Gwatkin and Guillot showed â€Å"58% of malaria deaths occurred in the poorest 20% of the world’s population, a higher percentage than any other disease of major public health importance†. Public health interventions intended to reach areas with people of low socioeconomic status may not be reaching their target population. Barat et al. ote that in developing countries, the poor â€Å"often live in the most remote areas and are socially or culturally marginalized† (http://www. cdc. gov/malaria/) Candida albicans- is a diploid fungus that grows both as yeast and filamentous cells and a causal agent of opportunistic oral and genital infections in humans and id the number one c ause of yeats infections in the U. S.. Candida albicans is commensal and a constituent of the normal gut flora comprising microorganisms that live in the human mouth and gastrointestinal tract. C. albicans lives in 80% of the human population without causing harmful effects. Candidiasis is often observed in immunocompromised individuals such as HIV-infected patients. A common form of candidiasis restricted to the mucosal membranes in mouth or vagina is thrush, which is usually easily cured in people who are not immunocompromised. To infect host tissue, the usual unicellular yeast-like form of C. albicans reacts to environmental cues and switches into an invasive, multicellular filamentous form, a phenomenon called dimorphism. Treatment is easily achieved by various medicines including antifungal drugs and topical ointments. Research Study- Recent research is still being conducted in hopes of finding a permanent means of dealing with Candida albicans and its resistance to certain drugs. Just within the last year, a Japanese university has taken the steps to specifically target the areas which allow the fungus to have resistance. They have observed that an ATP efflux inactivates the CDR1 and CDR2 genes which are responsible for drug resistance. Without the proper energy to activate the pump to rid of the antifungal agents, the resistance itself is in fact inoperable. The research team has also tried targeting other areas, such as stopping the production of mannan and glucan to prevent the structure of the cell wall. However, their main results show the cooperation between peptides and antifungal drugs. The results of this research will be used to treat other fungal and possible bacterial microbes that have drug resistant qualities (Antimicrobial peptides enhance the candidacidal activity of antifungal drugs by promoting the efflux of ATP from Candida cells. † Journal of Antimicrobial Chemotherapy. 2007) Cryptococcus neoformans- Is a round encapsulated yeast that causes meningitis in humans. The disease is acquired by coming in contact with contaminated soil but especially in solid that is contaminated with bird droppings. Cryptococcus neoformans reproduces by budding and produces spores that are then inhaled by a person. Once the dried fungi spores are inhaled the spread through out the central nervous system causing meningitis and severe lung infections. Cryptococcus neoformans is especially dangerous for immunocompromised individuals such as AIDS patients, and also has a mortality rate of 30%. Cryptococcus neoformans can be treated with an antifungal medicine called fluconazole. Research Study- Dendritic cells (DCs) play a pivotal role in host defense against invading pathogens including fungi, while DCs are targeted by fungi for deleterious regulation of the host immune response. A few studies have reported fungal modulation of DC function in these immunocompromised AIDS patients. Cryptococcus. neoformans (C. neoformans) is referred as one of the opportunistic fungi of AIDS. Here, researchers isolated native C. neoformans from an AIDS patient and investigated its effects on DC activation and How to cite Microbiology Research Paper, Essays