Infectious Episode of Streptococcus Pyogenes and Treatment

Infectious Episode of Streptococcus Pyogenes and TreatmentABCDMorphology way on AGARCocci. Cocci in clusters, short chains, diplococci and single cocci. Thin swabbed orange pigment from weighing machine. Surrounded by zones of clear beta-hemolysis.Cocci. Large round nauseated opaque grey colonies surrounded by zones of clear beta-hemolysis.Shiny.Bacilli. Small rod pale opaque grey colonies. Translucent. Shiny.Bacilli. Medium size colonies. Dark grey green. gibibyte ReactionPurple. Positive.Purple. Positive.Pink. Negative.Pink. Negative.OxidaseNegative.Positive.CatalaseNegative.Positive.CoagulasePositive.StrepGrouping LatexPositive for group A.Presumptive Identification?Streptococcus pyogenes. Staphylococcus aureus.Enterobacteria.genus Pseudomonas species.A = Streptococcus pyogenes. To further plump for that sample A is Streptococcus pyogenes you piece of tail undergo a PYR testing. The PYR test is a rapid colorimetric method which tests for the presence of the enzyme pyrrolid onyl aminopeptidase reach in the microorganism. The enzyme hydrolyses L-pyrrolidonyl--naphthylamide (PYR) to -naphthylamide, which produces a rosy-cheeked gloss when a cinnamaldehyde reagent is added. Paper strips atomic number 18 used to perform the test. A positive result for this test shows the typical morphology of S. pyogenes (Ferretti et al, 2016).Streptococcus pyogenes put forward as well as be tested by bacitracin test due to their sensitivity towards it. The test is used because other streptococci is resistant to bacitracin. A bacitracin test is undergone by making a subculture of the S. pyogenes on sheep blood agar. The bacterial push S. pyogenes being tested is streaked with individual colonies of a culture which is pure from an SBA agar plate and a disk containing 0.04 units of bacitracin is put onto the SBA plate. Incubation overnight at a temperature of 35C in CO2 (5%) then occurs. A zone of forbiddance surrounding the disc indicates the susceptibility of the st rain (Ferretti et al, 2016).B = Staphylococcus aureus. To further confirm that sample B is Staphylococcus aureus the ther almostable DNase test can be used. The thermostable DNAse test is performed using the agar diffusion method. 2ml aliquot of broth of the blood culture is boiled for a duration of 15 minutes and then allowed to cool to inhabit temperature. Holes of six-millimetres atomic number 18 cut in toluidine blue DNase agar plates. 100l of the boiled culture broth is placed into the well and then incubated at 37oC. Tests are read during 2 and 4 hours. The PPVs and NPVs for the culture is calculated as well as sensitivities and specificities. A result of 100% sensitivity means S. aureus is show (Lagace-Wiens et al, 2007).To reveal whether the strain is MSSA or MRSA a cefoxitin test is carried out. Susceptibility to cefoxitin is determined by the diffusion disc method on Mueller-Hinton agar plates. A suspension of the organisms is change to 0.5x MacFarland standard, dilut ed to 1100 and inoculated onto the Mueller-Hinton agar by streaking the agar surface all over. 30-g cefoxitin disks are applied and the plates are incubated at 37oC for 24 hours. An keep apart is an MRSA strain if the cefoxitin inhibition zone diameter is little than or equal to 21 mm (Boutiba-Ben Boubaker et al, 2004).C= Enterobacteria. To further confirm what enterobacteria sample c is, further tests need to be undertaken. To recognize if sample c is a type of Escherichia bacteria use the lipase test. The test sees if the bacteria uses corn oil as a source of one C and energy for growth. The result will be negative (if Escherichia) because the glossiness will be unchanged as no lipase is ease up (Vumicro.com, n.d.-b). To see if the sample is a Yersinia bacteria the lysine decarboxylase test can be used. The test sees if the bacteria can use lysine as a source of carbon and energy for growth. The result will be negative (if Yersinia) because of lack of colour change to yellow at 24 hours and back to purple at 48 hours (Vumicro.com, n.d.-c). To see if the sample is a Salmonella bacteria use the maltose test. The result will be negative (if Salmonella) due to magenta or hot bug in colour (Vumicro.com, n.d.-a). The citrate test needs to be undertaken to see if the sample is a Shigella bacteria. The test is a test used to assess the great power of the bacteria to utilize sodium citrate and ammonium dihydrogen phosphate. If the sample is a Shigella bacteria then the result for this test will be negative as there will be no colour change as the colour will stay deep forest green (Acharya, 2013).D = Pseudomonas species. To further confirm that sample D is Pseudomonas species a methyl red test can be used. The methyl red test is a test which detects the production of sufficient acid when glucose is fermented and the conditions are maintained such(prenominal) that the pH of the previous culture is kept below the value of 4.5, which is shown by the colour chang e of the methyl red indicator which is added when the period of incubation finishes. The result of this test for Pseudomonas species is negative because there is no change in colour when methyl red is added. The colour stays yellow (Online Microbiology Notes, 2014a).Another test that can be used is the voges-proskauer (VP) test. The test is a test used to see whether the pathogen produces acetylmethyl carbinol from glucose fermentation. If acteylmethyl carbinol is present it is converted to diacetyl in the presence of -naphthol, strong alkali and oxygen. Diacetyl found in the peptones in the broth is then condensed to form a pinkish red polymer. The result of this test for Pseudomonas species is negative because acetylmethyl carbinol is not present in Pseudomonas species (Online Microbiology Notes, 2014b).Infectious episode of Streptococcus pyogenes and treatmentStreptococcus pyogenes is one of the most important pathogens that cause skin and soft-tissue infections and is also assoc iated with septicaemia and other arduous complications (Segal et al, 2005). An example of a disease caused by Streptococcus pyogenes is ruddy febrility. Scarlet febricity is a contagious bacterial infection which affects children between 5 and 18 years old. It is spread by contact of droplets from the cough and sneezes of an infected psyche. Fever and thin-skinned throat is the first stage of illness. There also may be chills, vomiting and abdominal pain. The tongue is swollen and has a whitish coating. Throat and tonsils move around very red and sore, and swallowing becomes incredibly painful. After one or two days of the illness, a rash appears which is red in colour. Strep bacteria of the strain produce a toxin (poison) that causes people to break out in the rash. The rash appears first on the neck, underarm, and groin, which then spreads throughout the body. The rashes are small, flat red blotches that gradually change into fine bumps and feel like sandpaper. The cheeks have a flushed appearance, but there may also be a pale region around the mouth. Around the underarm, elbow, and groin the skin creases are brighter than the rest of the rash. These rashes are termed pastias lines. Complications of kidney damage, hepatitis, vasculitis, septicaemia, congestive heart failure and death may occur (Davis, n.d.). Scarlet fever can be treated with antibiotics. A strep test is needed. The test involves swabbing the throat to confirm whether group A streptococcus is creating the illness. If it is positive, prescription of antibiotics is needed. Antibiotics allows scarlet fever patients recover sooner and protect people from catching the disease (Centers for Disease Control and Prevention, 2017).Infectious episode of Staphylococcus aureus and treatmentStaphylococcus aureus can cause endocarditis. Endocarditis occurs when the bacteria adheres to the cardiac valve. bacterium can colonize the vegetation composed of fibrin and platelets (Keynan and Rubinstein, 2013). S. aureus enters the bloodstream due to healthcare procedures because of the dentogen pathway or drug use. Bacteria adhere extremely fast usually within minutes to an injured valve surface via deposition on platelet fibrin. It also adheres to inflamed valve surface. S. aureus enters via an intracellular passage to the valve endothelium which contributes to lighting and aggressive tissue destruction by the bacteria. The increase of bacteria on and in the endothelium leads to maturation of vegetation on the valve. Spreading of pathogens occurs from embolization of vegetation particles. This leads to complications such as stroke, haemorrhage, meningitis or reaction to the meningeal, brain abscess, and mycotic aneurysm (Werdan et al, 2013). There are many impacts of endocarditis which are physical and emotional. In the acute phase, unpleasant symptoms can be experienced which include high temperature, chills, loss of appetite, headache, muscle and joint pain, night sweats, shor tness of breath and persistent coughs. People who suffer from endocarditis experience complications of blood run to the brain which is affected. Worry and anxiety can occur which creates symptoms such as a racing heart, increased breathing rate, a dry mouth, sweating, tingling and shade dizzy. Low mood and depression also occurs because of endocarditis. When patients feel unwell and are being stuck in a hospital they can become sad. Feeling of hopelessness nearly the future and lacking in energy and drive can also occur. Struggling to enjoy the things you used to enjoy and feeling bad about yourself or criticised by others along with not being able to sleep or eat well occurs as well (Coping after Endocarditis, n.d.). Endocarditis is treated with a course of antibiotics or surgery (Nhs.uk, 2016).Infectious episode of Enterobacteria and treatmentEnterobacteria such as E. coli can cause gastroenteritis. E. coli enters the gastrointestinal tract and attaches to the facing of the in testinal mucosa where it secretes enterotoxins. Invasion of the intestinal mucosa does not occur. Toxins produced by the bacteria affect absorptions of nutrients and causes the cells of the intestinal mucosa to secrete electrolytes and water. Evidence of this will be in the form of profuse watery diarrhoea including vomiting which starts in 12 to 48 hours after ingestion. Other E. coli strains invade the cells of the mucosa and cause filtrate ulcers and bleeding. This creates inflammatory diarrhoea commonly associated with diarrhoea which sometimes can be bloody and there is a huge amount of abdominal pain. Toxins which E. coli produce present in foods causes secretory diarrhoea which is profuse and watery with nausea and vomiting that is very prominent. It is fast acting and symptoms may be evident in less than 12 hours after ingesting contaminated food. In some cases, the symptoms may be present in 1 to 6 hours. Patients with gastroenteritis have an increased risk for aortic ane urysm and ulcerative colitis (Ternhag et al, 2008). Treatments for gastroenteritis include antibiotics. Not every case of the disease needs antibiotics. Majority of cases of gastroenteritis are self-limiting and break apart in days. If the E. coli strain is associated with stool culture and persisting symptoms, then antibiotic treatment is needed. Patients which are immunocompromised also need antibiotics. Antidiarrheal agents can also be used to treat gastroenteritis. Antidiarrheal agents are used when symptoms are persisting even when antibiotics have been taken. The use of the agent is dependent on a case by case and needs to be consulted with a medical doctor before using an antidiarrheal agent. If a persistent diarrhoea is present then probiotics may also be needed (Chris, n.d.).Infectious episode of Pseudomonas speciesPseudomonas aeruginosa is the type specie for Pseudomonas which can cause bronchopneumonia. It is an inflammation of the lungs characterized by foci of consoli dation surrounded by normal parenchyma. Bronchopneumonia affects one or more lobes, being frequently bilateral and basal (Pathologyatlas.ro, 2014). When a person suffers from bronchopneumonia the lung parenchyma is attacked by the bacteria. An immune inflammatory response is triggered in response to this. Because of this, the alveolar sacs fill with ooze out. Consolidation then occurs when the air space is replaced by the exudate (fluid). Also there are multiple areas which is isolated of consolidation, affecting various pulmonary lobes (Hellomrdoctor.com, 2016). Lobular bronchopneumonia can lead to lobar pneumonia. Exudate starts to take up in the basal lobes. The affectation from this disease is bilateral. The lesions diameter vary between 2 and 4 cm and the lesions turn yellow or grey in colour, is dry and centred on a bronchiole. As well as this, their delimitation is not clear and the lesions become united. Suppurative exudate gathers due to inflammation in the bronchioles. A s more bronchioles suffer inflammation, the congestion experienced by the patient becomes more extensive. Between the areas of consolidation, the parenchyma remains normal and aerated (Hellomrdoctor.com, 2016). The effect of bronchopneumonia includes coughing and fever which makes breathing become difficult. If it is not treated mortality can be as high as 40%. If bronchopneumonia becomes severe the outer lining of the lungs and the inner lining of the chest becomes inflamed making breathing even more painful (Quinn, n.d.). If a person has bacterial bronchopneumonia antibiotics are prescribed. Antibiotics will destroy the bacteria causing the infection. Most people feel better within one to three days after starting antibiotics. Fever reducer or cough medication for bronchopneumonia may also be prescribed. These medications can help relieve symptoms, but does not redress the patient (Martel, 2015).BibliographyAcharya, T. (2013). Citrate utilization test Principle, Procedure, expec ted results and positive organisms microbeonline. Online microbeonline. functional at http//microbeonline.com/citrate-utilization-test-principle-procedure-expected-results-and-positive-organisms/ Accessed 28 Mar. 2017.Boutiba-Ben Boubaker, I., Ben Abbes, R., Ben Abdallah, H., Mamlouk, K., Mahjoubi, F., Kammoun, A., Hammami, A. and Ben Redjeb, S. (2004). Evaluation of a cefoxitin disk diffusion test for the enactment detection of methicillin-resistant Staphylococcus aureus. Clinical Microbiology and Infection, 10(8), pp.762-765.Centers for Disease Control and Prevention. (2017). Scarlet Fever. Online procurable at https//www.cdc.gov/Features/ScarletFever/ Accessed 12 Mar. 2017.Chris, D. (n.d.). What is Bacterial Gastroenteritis? Pathophysiology and Treatment Healthhype.com. Online Healthhype.com. operable at http//www.healthhype.com/what-is-bacterial-gastroenteritis-pathophysiology-and-treatment.html Accessed 13 Mar. 2017.Coping after Endocarditis. (n.d.). 1st ed. PDF London Im parts, pp.1-13. Available at https//www.kcl.ac.uk/ioppn/depts/pm/research/imparts/Quick-links/Self-Help-Materials/Coping-After-Endocarditis-(long).pdf Accessed 15 Mar. 2017.Davis, C. (n.d.). Scarlet Fever (Scarlatina) Symptoms, Treatment, Causes What is the prognosis of scarlet fever? What are the long-term effects of scarlet fever? MedicineNet. Online MedicineNet. Available at http//www.medicinenet.com/scarlet_fever_scarlatina/page4.htm Accessed 17 Mar. 2017.Ferretti, J., Stevens, D. and Fischetti, V. (2016). Streptococcus pyogenes Basic Biology to Clinical Manifestations. 1st ed. ebook okeh City University of Oklahoma Health Sciences Center, pp.875-891. Available at https//www.ncbi.nlm.nih.gov/books/NBK343617/ Accessed 10 Mar. 2017.Hellomrdoctor.com. (2016). Bronchopneumonia Symptoms, Pathophysiology, Diagnosis, Treatment. Online Available at http//hellomrdoctor.com/bronchopneumonia/ Accessed 13 Mar. 2017.Keynan, Y. and Rubinstein, E. (2013). Pathophysiology of Infective Endoc arditis. Current Infectious Disease Reports, 15(4), pp.342-346.Lagace-Wiens, P., Alfa, M., Manickam, K. and Karlowsky, J. (2007). Thermostable DNase Is Superior to piping Coagulase for Direct Detection of Staphylococcus aureus in Positive Blood Cultures. Journal of Clinical Microbiology, 45(10), pp.3478-3479.Martel, J. (2015). Bronchopneumonia. Online Healthline. Available at http//www.healthline.com/health/bronchopneumoniaOverview1 Accessed 13 Mar. 2017.Nhs.uk. (2016). Endocarditis Treatment NHS Choices. Online Available at http//www.nhs.uk/Conditions/Endocarditis/Pages/Treatment.aspx Accessed 15 Mar. 2017.Online Microbiology Notes. (2014a). Methyl Red (MR) Test- Principle, Procedure and Result Interpretation. online Available at http//www.microbiologyinfo.com/methyl-red-mr-test-principle-procedure-and-result-interpretation/ Accessed 17 Mar. 2017.Online Microbiology Notes. (2014b). Voges-Proskauer (VP) Test- Principle, Reagents, Procedure and Result. online Available at http//ww w.microbiologyinfo.com/voges-proskauer-vp-test-principle-reagents-procedure-and-result/ Accessed 17 Mar. 2017.Quinn, B. (n.d.). The effects of pneumonia. Online Telegraph.co.uk. Available at http//www.telegraph.co.uk/news/uknews/1553760/The-effects-of-pneumonia.html Accessed 22 Mar. 2017.Segal, N., Givon-Lavi, N., Leibovitz, E., Yagupsky, P., Leiberman, A. and Dagan, R. (2005). Acute Otitis Media Caused by Streptococcus pyogenes in Children. Clinical Infectious Diseases, 41(1), pp.35-41.Tong, S., Davis, J., Eichenberger, E., Holland, T. and Fowler, V. (2015). Staphylococcus aureus Infections Epidemiology, Pathophysiology, Clinical Manifestations, and Management. Clinical Microbiology Reviews, 28(3), pp.603-661.Ternhag, A., Trner, A., Svensson, ., Ekdahl, K. and Giesecke, J. (2008). Short- and Long-term effect of Bacterial Gastrointestinal Infections. Emerging Infectious Diseases, 14(1), pp.143-148.Vumicro.com. (n.d.-a). Maltose Fermentation Test. Online Available at http//www.vumic ro.com/vumie/help/VUMICRO/Maltose_Fermentation_Test.htm Accessed 28 Mar. 2017.Vumicro.com. (n.d.-b). Lipase (Corn Oil) Test. Online Available at http//www.vumicro.com/vumie/help/VUMICRO/Lipase_Corn_Oil_Test.htm Accessed 28 Mar. 2017.Vumicro.com. (n.d.-c). Lysine Decarboxylase Test. Online Available at http//www.vumicro.com/vumie/help/VUMICRO/Lysine_decarboxylase_Test.htm Accessed 28 Mar. 2017.Werdan, K., Dietz, S., Lffler, B., Niemann, S., Bushnaq, H., Silber, R., Peters, G. and Mller-Werdan, U. (2013). Mechanisms of infective endocarditis pathogen-host interaction and risk states. Nature Reviews Cardiology, 11(1), pp.35-50.