Saturday, January 25, 2020

The Many Infectous Diseases Caused by Streptococcus Pyogenes Essay

Streptococcus Pyogenes: Multi-Purpose Monsters Streptococcus pyogenes is a type of group A streptococci that causes many infectious diseases. This bacteria is commonly found in a variety of organisms, but is usually harmless unless the organisms defenses are compromised. When detrimental, group A streptococci cause infections such as impetigo, ecthyma, scarlet fever, and necrotizing fasciitis. Each of these infections displays different symptoms and requires different treatment. These treatments are primarily by antibiotics, because antibiotics are still the chief cure for GAS bacterial infections. One of the most interesting, rare, and fatal infections caused by streptococcus pyogenes is necrotizing fasciitis, and though it can cause some severe symptoms, a simple dose of antibiotics can prevent or even cure this dangerous infection. Streptococci are a large, diverse group of bacteria that are gram-positive cocci (Sharma). Streptococcus Pyogenes, a group A Streptococcus, is a universal organism that can cause many different diseases in humans (Sharma). Group A Streptococci are commonly referred to as GAS and they are commonly identified on blood agar plates as white or gray colonies (Sharma). They commonly appear in pairs or short chains that are non-motile and non-spore-forming (Sharma). Additionally, they have a fermentative metabolism, and are facultative anaerobes that require blood to grow (Todar). For this reason, GAS bacteria are often found in mammals. It is estimated that 15%-20% of all healthy individuals harbor this pathogen in their bodies, specifically their respiratory tract—without signs of disease (Todar). However, it is believed that the bacteria can cause harm if the organism’s defenses are compromised or th... ...July 2008 . DeLeo, Frank R., and Michael Otto. Bacterial Pathogenesis Methods and Protocols. Methods on Microbiology 431. Totowa, NJ: Humana Press, 2008. â€Å"Necrotizing Fasciitis (Flesh-Eating Bacteria).† WebMD. 6 Dec. 2007. Healthwise Inc. 14 July 2008 . Rene, Caravano. Current Research on Group A Streptococcus . Paris, France: Excerpta Medica Foundation, 1968. Sharma, Sat, MD. â€Å"Streptococcus Group A Infections.† eMedicine. 5 May 2006. WebMed. 24 July 2008 . Todar, Kenneth. â€Å"Streptococcus Pyogenes.† Todar’s Online Textbook of Bacteriology. 2002. University of WIsconsin-Madison. 14 July 2008 .

Friday, January 17, 2020

Causes Of Myasthenia Gravis Health And Social Care Essay

Myasthenia Gravis is an autoimmune upset, the immune system attacks portion of the organic structure. In MG that portion is the muscular system. The organic structure produces antibodies that mark receptors for the neurotransmitter acetylcholine on the musculus cells at neuromuscular junctions. Peoples with MG have a one -third the normal figure of acetylcholine receptors here. On a whole -body degree, this causes weak and easy fatigued musculuss. MG affects 100s of 1000s of people worldwide. Mostly adult females in their mid-twentiess or mid-thirtiess, and work forces in their 1960ss and 1970ss. The particular symptoms depend upon the site of onslaught. For 85 % of patients, the disease causes generalised musculus failing. Many people develop a characteristic level smiling and rhinal voice and have trouble mastication and get downing due to affected facial and neck musculuss. Many have limb failing. About 15 % of patients experience the unwellness merely in the musculuss environing their eyes. The disease reaches crisis degree when respiratory musculuss are affected, necessitating a ventilator to back up external respiration. MG does non impact esthesis or physiological reactions ( Shier, 2010 ) . Causes of Myasthenia Gravis The exact cause of MG is non known. One theory is the status may be triggered by a virus or other infection that has a similar construction to a portion of the acetylcholine receptor. Sometimes adult females with MG who give birth transmit these peculiar antibodies to their babes, doing musculus failing in the baby. This is called neonatal myasthenia and occurs in approximately 12 % of babes whose female parent has MG. â€Å" It is different from inborn myasthenia because the infant gets better in a few hebdomads as the antibody blood degrees go down † ( MediResource, 2013 ) . The other abnormalcy that frequently shows up in people with myasthenia gravis is an hyperactive, overlarge, or otherwise nonfunctional Thymus. The Thymus is a secretory organ located where the cervix joins the thorax. It is of import for the normal development of the immune system. Normally, the Thymus is larger in childhood than in maturity and becomes inactive around pubescence. In people with MG, nevertheless, it frequently keeps traveling into maturity ( MediResource, 2013 ) . Some people with MG turn out to hold a thymoma ( a tumour in the Thymus ) . This is a type of malignant neoplastic disease, but really few people die of thymomas ( MediResource, 2013 ) . The most common symptoms of MG are the dual vision which is called diplopia, every bit good as saging palpebras which is called ptosis, and musculus failing that normally gets worse after exercising or at the terminal of the twenty-four hours and improves with remainder. ` Swallowing troubles are of peculiar concern as they can be unsafe. MG typically does good at the beginning of a repast but tyre at the terminal, do get downing excessively hard. Some deteriorate to name where there is entire loss of ability to masticate and get down. At this point, nutrient may lodge in the pharynx, or nutrient and drink may get down to travel the incorrect manner, for illustration into the trachea, doing coughing and choking. Foods which may trip MG symptoms may be: Very hot, Spicy, Dry and britty Foods which require a batch of masticating attempt, such as tough meats or chewy Sweets, could besides pall out the myasthenic and cause trouble in get downing ( Boyce, 2013 ) . Many people with MG upset find it temporarily impossible to eat may hold to be admitted to a infirmary and be fed intravenously. Of more immediate danger is when the disease causes trouble in breathingaˆÂ ¦This is called a myasthenic crisis, and it ‘s responsible for most of the little figure of deceases due to myasthenia gravis. Peoples with take a breathing jobs must travel to a infirmary instantly. ( Boyce, 2013 ) How is Myasthenia Gravis treated? Today, MG can be controlled. There are several therapies available to assist cut down and better musculus failing. Medicines used to handle the upset include anticholinesterase agents such as Prostigmin and pyridostigmine, which help better neuromuscular transmittal and increase musculus strength. Immunosuppressive drugs such as Orasone, cyclosporine, and Imuran may besides be used. These medicines improve musculus strength by stamp downing the production of unnatural antibodies. They must be used with careful medical followup because they may do major side effects ( Nursing Link, 2013 ) . What is the forecast? With intervention, the mentality for most patients with MG is bright: they will hold important betterment of their musculus failing and they can anticipate to take normal or about normal lives. Some instances of MG may travel into remittal temporarily and muscle failing may vanish wholly so that medicines can be discontinued. Stable, durable complete remittals are the end of thymectomy. In a few instances, the terrible failing of MG may do a crisis which requires immediate exigency medical attention ( Nursing Link, 2013 ) . How is Myasthenia Gravis Diagnosed? The first stairss of naming MG include a reappraisal of the person ‘s medical history, and physical and neurological scrutinies. The marks a doctor must look for are impairment of oculus motions or musculus failing without any alterations in the person ‘s ability to experience things. If the physician suspects MG, several trials are available to corroborate the diagnosing. A particular blood trial can observe the presence of immune molecules or acetylcholine receptor antibodies. Most patients with MG have abnormally elevated degrees of these antibodies. However, antibodies may non be detected in patients with lone optic signifiers of the disease ( Nursing Link, 2013 ) . Another trial is called the edrophonium trial. This attack requires the endovenous disposal of edrophonium chloride or tensionA ® , a drug that blocks the debasement ( breakdown ) of acetylcholine and temporarily increases the degrees of acetylcholine at the neuromuscular junction. In people with MG affecting the oculus musculuss, edrophonium chloride will briefly alleviate failing. Other methods to corroborate the diagnosing include a version of nervus conductivity survey which trials for specific musculus â€Å" weariness † by insistent nervus stimulation. This trial records weakening musculus responses when the nervousnesss are repetitively stimulated. Insistent stimulation of a nervus during a nervus conductivity survey may show decreases of the musculus action potency due to impaired nerve-to-muscle transmittal ( Nursing Link, 2013 ) . The Future The hereafter of Myasthenia Gravis lies in the elucidation of the molecular immunology of the anti-acetylcholine receptor response with the end of developing a rational intervention for the unwellness that will bring around the abnormalcy in the immune system that consequences in the AChR immune response. To this terminal, six wide classs of theoretical intervention schemes need to be explored. First, those interventions which target the antigen specific B-cells ; Second, those interventions which target the antigen specific CD4+ T-cells ; Third, those interventions which interfere with co-stimulatory response for antigen presentation, Fourth, interventions aimed at bring oning tolerance or anergy of the CD4+ T-cell to the car antigen or the CD4+ epitopes ; Fifth, those interventions designed to excite those immunological circuits which activate CD8+ cells specific for the activation antigens expressed by CD4+ cells and Sixth, those interventions which intervene with cytokine map and discourage autoimmune mediated inflammatory responses ( Howard, 2010 ) .

Wednesday, January 8, 2020

Abnormal Invasion Of Their Personal Space - 851 Words

In this social norm project, my experiment was invading someone else s personal space. The process began by sitting close to a person that was by themselves; then, I started to get close when they looked to another direction or their phones. What normally a person would do when they tired or they want to sit, they mostly sit apart from a stranger or they sit with a distance between them. What I did in my project is that I sat close to a stranger when there is space where I could go and sit. The purpose for this project is to see their reactions and response with these abnormal invasion of their personal space. Before I started to do my project, I had trouble to put myself together when it came the time to start to sit beside someone I didn’t know because I was nervous about their response and reaction by invading their space. After reflecting and putting myself together I sat beside strangers; the responses weren’t unacceptable as I though before the encounter. 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