Infective Endocarditis Caused by Viridans Streptococci

infectious Endocarditis Caused by Viridans StreptococciCase Study 1 Infective endocarditis caused by viridans strepCase Study 2 haemorrhagic fever caused by EbolavirusCase Study 1Subject is a 48-year-old man with a sexual conquest statement of mitral valve regurgitation who presents with a 10-day history of fatigue, fever and oecumenical malaise. nearly reddish lesions atomic number 18 noned on his palm, which he has never noticed before. He denies any cough, scarcely has bonkers new shortness of breath with exertion and with lying down matted at night in bed.He is generally in nigh(a) health except for a root canal operation around 3 weeks previously. The history of mitral valve regurgitation is thought to be minuteary to rheumatic fever as a child. Heart examination is guiding light for a loud systolic murmur best heard at the left sternal border with radiation over to the axilla. Lungs be undefendable and abdominal examination is normal. Skin examination is signi ficant for several mixed-up reddish lesions over his palms and soles that atomic number 18 not painful when pressure is applied. science laboratory tests Blood wait shows WBC 14.8 with 86% neutrophils blood cultures grew give away positive cocci in chains that be alpha haemolytic on horse blood agar.Evidence for DiagnosisMitral valve regurgitation would account for the fatigue, and as well as the shortness of breath in the patient, however another(prenominal)(a) symptoms be present that this alone cannot explain. The first of these is the fever suffered by the patient, which would signify an contagion. The second is the presence of lesions on the palms and soles Petechiae such(prenominal) as these, cognise as Janeway lesions, are an indicator of endocarditis (OConnor, 2002), and the patients history of mitral valve regurgitation, along with a recent history of root canal work confirm that this is a likely diagnosing. The lungs and abdomen of the patient are clear, as woul d be anticipate in a case of endocarditis, however examination of the heart sounds displayed a clear murmer. The patients blood imports showed clear signs of infection, with leukocytosis and elevated neutrophil count. The bacteria cultured from the patients blood can be easily identified as Streptococci, and since this is known to be a tributary be of endocarditis (Brooks, Butel and Morse, 2004, pp.197), it makes the diagnosis very(prenominal) likely.Further Testing Required succession the diagnosis in this case should be straight forward callable to bacteraemia and presence of peripheral stigmata, according to the Duke criteria, which is used as a scape for diagnosis of infectious endocarditis, this patient would be classified as having solo workable infective endocarditis. As they display nigh of the necessary pathological and clinical criteria, they would need advertise tests to determine if it was definitely infective endocarditis (Li et al., 2000). The Duke Criter ia was positive by Durack et al. (1994) as a means of better distinguishing infective endocarditis from other causes of cardiac problems these were evaluated as being superior to previous methods for diagnosis (aspirin et al., 1994)(Cecchi et al., 1997)(Hoen et al., 1995) The criteria strike been used since, though thither have been studies done into improving the criteria except. gibe to these criteria, the patients diagnosis could be confirmed by carrying out other tests such as an ECG, echocardiogram, and chest x-ray, to exclude other possible cardiac problems. However, the patient would also meet cardinal major criteria, and wherefore be classified as definite infective endocarditis if two further cultures of blood grew causative bacteria. objet dart the most likely causative organism is viridans streptococci, as Streptococcus pneumonia is to a greater extent commonly associated with bacterial pneumonia or meningitis, the two can be differentiated quite simply by scrutin y with optochin. S. pneumonia are susceptible to this microbial agent, where viridans streptococci are resistant. Suspending the bacteria in bile salts would also provide a suitable distinction, as S. pneumonia would lyse, where viridans streptococci are insoluble (Brooks, Butel and Morse, 2004, pp.197).Endocarditis as a consequent of streptococcal infectionMicrobiologyMany textbooks, and in fact some journal articles refer to the assemblage of streptococci which cause endocarditis by the name Streptococcus viridans, however this is actually a misnomer, as the viridans streptococci are actually a assort of several different bacteria, and are referred to as viridans simply because they produce a green halo when grown on blood agar (Elliott et al., 1997, pp.30-1).Viridans streptococci are often found resident in abundance in the mouth, where they are usually commensal, or cause only mild infections formerly in the blood stream, these usually passive bacteria can die pathogenic, and lead to endocarditis upon reaching the heart (Brooks, Butel and Morse, 2004, pp.197). The bacteria are able to grow in structurally abnormal valve surfaces and gradually lead to the destruction of the valves, caseing in regurgitation (OConnor, 2002). Those valves damaged by rheumatic fever are oddly prone to infection (Heritage, Evans and Killington, 1999, p.185).SymptomsThe physical symptoms suffered by the patient are a result of the physical structures response to the infection the fever and general malaise suffered by the patient would be as a result of cytokine generation from the number one-grade infection, and the petechiae in the skin, known as Janeway lesions, are the result of immune complexes being deposited in small vessels thither (OConnor, 2002).ProphylaxisAny patient, such as the one here, assessed from their previous medical history to be at risk from endocarditis, should be inclined prophylactic intercession before undergoing incursive dental surgery. Th e current guidelines outlined by Ramsdale et al. (2004) recommend amoxicillin for this purpose, or clindamycin for those allergic to penicillin. This particular patient would only be considered a confine risk according to the new guidelines, so there would be no need for gentamicin, however those considered at high risk would be given this intravenously in addition to IV amoxicillin/clindamycin.TreatmentA combination of penicillin and gentamicin are used to treat streptococcal endocarditis. While studies have found that there is only a limited safeguard to penicillin in sufferers at present, vancomycin can be used a viable alternative in those allergic to penicillin and those with more resistant strains (Johnson et al., 2001).For those who do not respond to antimicrobial treatment, surgery is often a viable option, replacing the infected valves. While not of all time prospered, this offers an improved aspect for those where other treatment is unsuccessful (Moon et al., 1997).Pr ognosisIf left untreated, infective endocarditis is always fatal, as the destruction of a valve will pr level offt the heart from working. notwithstanding if treated, the ailment carries a high morbidity and mortality rate. The factors which impact strongest on prognosis are un hold inled infection and congestive heart failure. It is for this discernment that early diagnosis and antimicrobial treatment is necessary. However, constant improvements in operative procedures are leading to a better prognosis for those not responding to treatment (Karth et al., 2002). It could be reasoned that these advances in surgery will become even more important in prognosis as incidences of antimicrobial tube increase, which is surely inevitable judging by trends in other bacterial infections such as Staphylococcus aureus.Case Study 4A 34-year-old woman researcher studying chimpanzee behaviour in the pearl Coast found several of the animals were dying. She dissected one several hours later it died and found that it had died of haemorrhage, and had non- turn blood. She wore household gloves, but no mask or habilitate during the dissection. Eight days later she developed a fever and headache, which did not respond to malaria treatment. Five days into her illness, she developed vomiting, diarrhoea, a rash, and renal failure. Antibiotics did not improve her condition and she was transported home in isolation.The patient is lethargic but communicative. She has lymphadenopathy. Her lung exam is normal. She has a mildly tender and enlarged coloured and spleen.research laboratory tests She has a white blood cell count of 3.6, haematocrit of 40, and low platelets of 83. She has a low fibrinogen of 0.8. Her clotting times are normal, however. serological tests for anthrax, dengue fever, chikungunya, yellow fever, Crimean-Congo haemorrhagic fever, Marburg virus, Rift Valley fever, Lassa fever, and Hantavirus are all negative.Evidence for DiagnosisThe history of the patient sugges ts that she is pathetic from something that has arisen from her nexus with an infected chimpanzee. While a number of zoonotic complaints are known to be prevalent in the African continent, the majority of those have already been ruled out by negative test results. One which has not is the Ebolavirus, which gives rise to Ebola haemorrhagic fever. infection of the Ebolavirus from dead animals has been documented in the past, including in the Ivory Coast (WHO, 2004 CDC, 2005).The onset of the patients symptoms fits with the known timescale for the Ebolavirus of 2 to 21 days the fever and headache which she experienced are continent symptoms. Later in the disease sufferers also usually develop diarrhoea, vomiting, and possibly a rash (CDC, 2005). It would obviously be expected that antibiotics would bring no improvement to the illness, as the infection is viral.In a physical examination, it would be expected that a patient infected with Ebolavirus would have an enlarged liver and spleen, as this is where virus replication is particularly proliferant. Sanchez et al. (2004) also specifies the lungs as also being one of the main sites of virus replication, implying that the patient should be suffering from tenderness of the lungs also, however this evidence is taken from studies into the Sudan strain of Ebolavirus, and this is much more likely to be the Ivory Coast strain, so some symptoms may differ.In the laboratory examination, it is expected to see a normal haemocrit, accompany by leucopenia and thrombocytopenia as displayed in the patient. It would be usual for the clotting time to be shortened, however this patient has low levels of fibrinogen, possibly ascribable to some secondary cause, which may alter the clotting time, making it high than expected.Further Testing RequiredWhile virus isolation, transmission negatron microscopy, immunohistochemistry, reverse transcription-PCR, antigen capture enzyme-linked-immunosorbent serologic assay, and IgG or IgM antibody capture ELISA can all been used to show Ebolavirus as the causitive agent, there are conflicting storys over which techniques are preferable for use. The Centres for disorder Control and barroom (2005) suggest that in a patient at this stage of the disease, examination should be carried out for IgM and IgG antibodies, Kurosaki et al. (2006) and Towner et al. (2004) recommend RT-PCR as the most efficient technique.EbolavirusAetiologyEbola belongs to the filoviruses or Filoviridae, which is divided into two genera, the Ebolavirus and the Marburgvirus. The Ebolavirus genus is divide into four separate species Ivory Coast ebolavirus, Sudan ebolavirus, Zaire ebolavirus and Reston ebolavirus (Hensley et al., 2005). While the disease is zoonotic, the natural reservoir of the disease is not non- valet primates the actual reservoir and the mode of transition into apes is so far unknown, although studies are currently being undertaken on the suggestion that bats may play a r ole. Transmission into humans is rare, and is often one isolated case (Peterson et al., 2004), although if the proper precautions are not taken it is possible for the disease to spread in the human population.EpidemiologyThe disease has appeared sporadically since its initial recognition in 1976, and has occurred only in specific geographicalal areas as per the names of the different strains (CDC, 2005). It is generally concur that the virus is transmitted via direct contact with the blood or visible secretions from another infected person (Dowell et al., 1999 WHO, 2004), due to the extensive viral affaire in the subcutaneous weave (Peters, 2005). It is believed that this is also the case among non-human primates, such as the chimpanzees, although this is so far unconfirmed (CDC, 2005). In laboratory studies, the virus has shown the magnate to be spread via aerosol between rhesus monkeys (Johnson et al., 1995), and while some authors such as Heeney (2006) list the virus as bei ng aerosol, there have so far been no such documented cases in a real-world context of use between humans (CDC, 2005 Dowell et al., 1999).SymptomsThe World health government activity (2004) lists the main symptoms of the Ebolavirus as being a sudden onset of fever, attended by intense weakness and muscle pain, headaches and a sore throat. by and by a few days this is followed by vomiting and diarrhoea, rashes, liver and kidney dysfunction and sometimes also some(prenominal) internal and external bleeding.PathogenesisThe pathogenesis of Ebolavirus is currently very hard to study, due to the rarity of occurrences in humans, and also due to the weighty nature of collecting, storing and analysing samples from those cases. The illness is severe due to the ability of the virus to supress both adaptive and innate immune responses, and the ability to cause extreme rabble-rousing responses and intravascular coagulation (Mahanty and Bray, 2004).At the current time it is thought that m onocytes and macrophages in the body are infected during the early stages of the virus, and these then carry the virus to other areas (Sanchez et al., 2004). The infected monocytes express large amounts of tissue factor, leading to intravascular coagulation, and causing tissue damage. Infected macrophages secrete cytokines which cause apoptosis of lymphocytes in tissues that are needed for the acquired immune response (Peters, 2005), hence the presence of leucopenia in blood count results. The mobile infected cells carry the viral agent to lymph nodes, where the virus further replicates and is spread through the body. Upon reaching the liver, spleen and other tissues, parenchymal cells, including hepatocytes and adrenal cortical cells will become infected (Mahanty and Bray, 2004). This is what leads to the enlarged organs, and will also result in an increase in the levels of liver enzymes in the blood.Prophylaxis and TreatmentSome progress has been made in the formation of vaccines , and these have proved successful in testing on non-human primates (Hensley et al., 2005). However other sources report that all attempts so far have met with outright failure (Peters, 2005). barrier nursing techniques appear to be effective in preventing the spread of the disease (Dowell et al., 1999 Formenty et al., 1999).PrognosisThe Zaire strain of Ebolavirus is reportedly the most lethal (Mahanty and Bray, 2004) there is only one reported case of a human detection the Ivory Coast strain, presenting similarly to the patient, and they survived (Formenty et al., 1999). It is very difficult to form an perfect prognosis however due to the limited results on which to base it.ReferencesBayer A.S., Ward J.I., Ginzton L.E. and Shapiro S.M. (1994) Evaluation of new clinical criteria for the diagnosis of infective endocarditis. American ledger of Medicine, 96 (3), pp.220-2Brooks G.F., Butel J.S. and Morse S.A. (2004) Medical Microbiology 23rd Edition. McGraw-Hill, p.197CDC (2005) Cen tres for Disease Control and Prevention online- November 18, 2005.- available from http//www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/ebola/qa.htm cited February 2, 2007Cecchi E., Parrini I., Chinaglia A., Pomari F., Brusasco G., Bobbio M., Trinchero R. and Brusca A. (1997) peeled diagnostic criteria for infective endocarditis. A study of sensitivity and specificity Eureopean Heart Journal, 18 (7), pp. 1149-56Dowell S. F., Mukunu R., Ksiazek T. G., Khan A. S., Rollin P. E. and Peters C. J. 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