Infective Endocarditis Caused by Viridans Streptococci

Infective Endocarditis Caused by Viridans StreptococciCase Study 1 Infective endocarditis caused by viridans streptococcusCase Study 2 Haemorrhagic fever caused by Ebolacomputer virusCase Study 1Subject is a 48-year-old valet with a history of mitral valve vomiting who presents with a 10-day history of fatigue, fever and general malaise. Some reddish lesions argon noned on his palm, which he has never noticed before. He denies any cough, but has mild fresh shortness of breath with exertion and with lying down flat at night in bed.He is generally in good health except for a infrastructure canal operation approximately 3 weeks previously. The history of mitral valve regurgitation is thought to be secondary to rheumatic fever as a child. Heart examination is notable for a loud systolic murmur beat out heard at the left sternal border with radiation over to the axilla. Lungs atomic number 18 clear and abdominal examination is normal. Skin examination is significant for several(pre nominal) scattered reddish lesions over his palms and soles that are not painful when pressure is applied.Lab tests Blood count shows WBC 14.8 with 86% neutrophils agate line cultures grew out Gram-positive cocci in chains that are alpha haemolytic on horse rip agar.Evidence for DiagnosisMitral valve regurgitation would account for the fatigue, and in addition the shortness of breath in the patient, thus far other symptoms are present that this alone cannot explain. The first of these is the fever suffered by the patient, which would signify an infection. The second is the presence of lesions on the palms and soles Petechiae such as these, known 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 in all likelihood diagnosing. The lungs and abdomen of the patient are clear, as would be expected in a pillow slip of endocarditis, however examination of the heart sounds displayed a clear murmer. The patients blood numbers 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 causative organism of endocarditis (Brooks, Butel and Morse, 2004, pp.197), it makes the diagnosing very likely.Further Testing unavoidableWhile the diagnosis in this case should be straight forward due to bacteraemia and presence of peripheral stigmata, according to the Duke criteria, which is used as a shot for diagnosis of infective endocarditis, this patient would be classified as having only attainable infective endocarditis. As they display some of the necessary pathologic and clinical criteria, they would need only tests to determine if it was definitely infective endocarditis (Li et al., 2000). The Duke Criteria was vexed by Durack et al. (1994) as a means of better distinguishing infec tive endocarditis from other causes of cardiac problems these were evaluated as organism superior to previous methods for diagnosis (Bayer et al., 1994)(Cecchi et al., 1997)(Hoen et al., 1995) The criteria have been used since, though at that place have been studies done into improving the criteria further. According to these criteria, the patients diagnosis could be confirmed by continueing out other tests such as an ECG, echocardiogram, and chest x-ray, to exclude other possible cardiac problems. However, the patient would also bear upon two major criteria, and therefore be classified as definite infective endocarditis if two further cultures of blood grew causative bacteria.While the most likely causative organism is viridans strep, as Streptococcus pneumonia is more commonly associated with bacterial pneumonia or meningitis, the two can be polariated quite simply by examination with optochin. S. pneumonia are susceptible to this microbial agent, where viridans streptococci a re kind. 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 result of streptococcal infectionMicrobiologyMany textbooks, and in fact some journal articles refer to the group of streptococci which cause endocarditis by the name Streptococcus viridans, however this is actually a misnomer, as the viridans streptococci are actually a group 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 effect resident in abundance in the mouth, where they are usually commensal, or cause only mild infections once in the blood stream, these usually still bacteria can become pathogenic, and carry on to endocarditis upon reaching the heart (Brooks, Butel and Morse, 2004, pp.197). The bacteria are able to proliferate in structurally abnormal valve surfaces and gradually lead to the destruction of the valves, resulting in regurgitation (OConnor, 2002). Those valves damaged by rheumatic fever are particularly prone to infection (Heritage, Evans and Killington, 1999, p.185).SymptomsThe physical symptoms suffered by the patient are a result of the bodys response to the infection the fever and general malaise suffered by the patient would be as a result of cytokine generation from the low-grade infection, and the petechiae in the skin, known as Janeway lesions, are the result of immune complexes being deposited in small vessels there (OConnor, 2002).ProphylaxisAny patient, such as the one here, assessed from their previous medical history to be at risk from endocarditis, should be given prophylactic treatment before undergoing invasive dental surgery. The up-to-the-minute guidelines outlined by Ramsdale et al. (2004) recommend amoxicillin for this purpose, or clindamycin for those allerg ic to penicillin. This particular patient would only be considered a moderate 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 resistance to penicillin in sufferers at present, vancomycin can be used a viable metamorphosenative 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 always successful, this offers an improved panorama for those where other treatment is unsuccessful (Moon et al., 1997).PrognosisIf left untreated, infective endocarditis is always fatal, as the destruction of a valve will prevent the heart from working. Even if treated, the distemper carries a high morbidity and mortality rate. The factors which impact strongest on prognosis are uncontrolled infection and congestive heart failure. It is for this reason that early diagnosis and antimicrobial treatment is necessary. However, constant improvements in surgical 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 resistance 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 Ivory Coast found several of the animals were dying. She dissected one several hours after it died and found that it had died of haemorrhage, and had non-clotting blood. She wore household gloves, but no mask or gown during the dissectio n. 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 liver and spleen.Lab 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, color fever, Crimean-Congo haemorrhagic fever, Marburg virus, Rift Valley fever, Lassa fever, and Hantavirus are all detrimental.Evidence for DiagnosisThe history of the patient suggests that she is suffering from something that has arisen from her contact with an infected chimpanzee. While a number of zoonotic diseases 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. Transmission 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 classic 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 briny sites of virus re plication, 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, accompanied 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 due to some secondary cause, which may alter the clotting time, making it higher than expected.Further Testing RequiredWhile virus isolation, transmission electron microscopy, immunohistochemistry, retrovert transcription-PCR, antigen capture ELISA, and IgG or immunoglobulin M antibody capture ELISA can all been used to show Ebolavirus as the causitive agent, there are conflicting reports over which techniques are preferable for use. The Centres for Disease go for and Prevention (2005) suggest that in a patient at this stage of the disease, testing 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 split into four separate species Ivory Coast ebolavirus, Sudan ebolavirus, Zaire ebolavirus and Reston ebolavirus (Hensley et al., 2005). While the disease is zoonotic, the inbred reservoir of the disease is not non-human primates the actual reservoir and the mode of transition into apes is so far unknown, although studies are currently being undertaken on the prompt that bats may play a role. 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 populatio n.EpidemiologyThe disease has appeared sporadically since its initial recognition in 1976, and has occurred only in specialised geographical areas as per the name of the different strains (CDC, 2005). It is generally agreed that the virus is transmitted via direct contact with the blood or bodily secretions from another infected person (Dowell et al., 1999 WHO, 2004), due to the big viral involvement in the subcutaneous tissue (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 king to be spread via aerosol between rhesus monkeys (Johnson et al., 1995), and while some authors such as Heeney (2006) list the virus as being aerosol, there have so far been no such documented cases in a real-world setting between humans (CDC, 2005 Dowell et al., 1999).SymptomsThe World health fundamental law (2004) lists the main symptoms of the Eb olavirus as being a sudden onset of fever, accompanied by intense weakness and muscle pain, headaches and a sore throat. After a few days this is followed by vomiting and diarrhoea, rashes, liver and kidney dysfunction and sometimes also both internal and external bleeding.PathogenesisThe pathogenesis of Ebolavirus is currently very hard to study, due to the quirkiness of occurrences in humans, and also due to the dangerous 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 inflammatory responses and intravascular coagulation (Mahanty and Bray, 2004).At the current time it is thought that monocytes 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 intrava scular coagulation, and causing tissue damage. Infected macrophages secrete cytokines which cause apoptosis of lymphocytes in tissues that are required 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 effect ive 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 contracting the Ivory Coast strain, presenting similarly to the patient, and they survived (Formenty et al., 1999). It is very difficult to form an accurate 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) paygrade of new clinical criteria for the diagnosis of infective endocarditis. American Journal of Medicine, 96 (3), pp.220-2Brooks G.F., Butel J.S. and Morse S.A. (2004) Medical Microbiology twenty-third Edition. McGraw-Hill, p.197CDC (2005) Centres 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., B obbio M., Trinchero R. and Brusca A. (1997) New 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. (1999) Transmission of Ebola hemorrhagic fever A study of risk factors in family members, Kikwit, Democratic Republic of the Congo, 1995. Journal of infective Disease, 179 Suppl. 1, pp. S87-S91Durack D.T., Lukes A.S. and Bright D.K. (1994) New criteria for diagnosis of infective endocarditis utilization of specific echocardiographic findings, American Journal of Medicine, 96 (3), pp. 200-9Elliott M., Hastings U., Desselberger R. and Reid G. (1997) Lecture Notes on Medical Microbiology Oxford, UK Blackwell Publishing, pp.30-1Formenty P., Hatz C., Le Guenno B., Stoll A., Rogenmoser P. and Widmer A. (1999) Human infection due to Ebola virus, subtype Cote dIvoire Clinical and biologic presentation. Journal of Infectious Diease, 17 9 Suppl. 1, pp.S48-S53Heeney J.L. (2006) Zoonotic viral diseases and the frontier of early diagnosis, control and prevention. Journal of Internal Medicine, 260, pp. 399-408Hensley L., Jones S., Feldmann H., Jahrling P. and Geisbert T. (2005) Ebola and Marburg viruses Pathogenesis and development of countermeasures. Current Molecular Medicine, 5, pp. 761 772Heritage J., Evans E.G.V. and Killington R.A. (1999) Microbiology in Action. Cambridge, UK Cambridge University Press, p. 185Hoen B., Selton-Suty C., Danchin N., Weber M., Villemot J.P., Mathieu P., Floquet J. and Canton P. (1995) Evaluation of the Duke criteria versus the Beth Israel criteria for the diagnosis of infective endocarditis. Clinical Infectious Disease,21 (4), pp. 905-9Johnson A.P. et al. (2001) Antibiotic susceptibility of streptococci and related genera causing endocarditis analysis of UK reference laboratory referrals, January 1996 to March 2000. BMJ, 322, p. 7283Johnson E., Jaax N., White J. and Jahrling P. (1995 ) lethal experimental infections of rhesus monkeys by aerosolized Ebola virus. International Journal of Experimental Pathology, 76 (4), pp. 227-236Karth G.D. et al. (2002) Complicated infective endocarditis necessitating ICU admission clinical course and prognosis. unfavorable Care, 6 (2), pp. 149 154Kurosaki Y., Takada A., Ebihara H., Grolla A., Kamo N., Feldmann H., Kawaoka Y. and Yasuda J. (2006) Rapid and simple detection of Ebola virus by reverse transcription-loop-mediated isothermal amplification. Journal of Virological Methods, doi 10.1016.Li J.S., Sexton D.J., Mick N., Nettles R., Fowler V.G., Ryan T., Bashore T. and Corey G.R. (2000) Proposed modifications to the Duke Criteria for the diagnosis of Infective Endocarditis. Clinical Infectious Disease, 30, pp.633-638Mahanty S. and Bray M. (2004) Pathogenesis of filoviral haemorrhagic fevers. The Lancet, 4 (8) pp. 487-498Moon M.R., Stinson E.B. and Miller D.C. (1997) Surgical treatment of endocarditis. Progress in Cardiovas cular Diease, 40 (3) pp. 239-64OConnor D. (2002) Pathology. Elsevier Health SciencesPeters C. J. (2005) Marburg and Ebola Arming ourselves against the deadly filoviruses. New England Journal of Medicine, 325 (25), pp. 2571-2573.Peterson A.T., Bauer J.T. and Mills J.N. (2004) Ecologic and geographic distribution of filovirus disease. Emerging Infectious Dieases, 10 (1), pp. 40-7.Ramsdale D.R. et al (2004) Dental aspects of Endocarditis Prophylaxis New Recommendations from a Working sort out of the British Cardiac Society Clinical Practice Committee and Royal College of Physicians Clinical Effectiveness and Evaluation Unit Report Working Group of the British Cardiac Society Clinical Practice Committee and Royal College of Physicians Clinical Effectiveness and Evaluation, 19 April 2004.Sanchez A., Lukwiya M., Bausch D., Manharty S., Sanchez A., Wagoner K. and Rollin P. (2004) Analysis of human peripheral blood samples from fatal and nonfatl cases of Ebola (Sudan) haemorrhagic fever Cellular responses, virus oad and nitric oxide levels. Journal of Virology, 78 (19), pp.10370-10377.Towner J.S. et al. (2004) Rapid diagnosis of Ebola hemorrhagic fever by reverse transcription-PCR in an outbreak setting and assessment of patient viral load as a predictor of outcome. Journal of Virology, 78 (8), pp. 4330-4341WHO (2005) World Health Organisation Ebola Factsheet Onlineavailable at http//www.who.int/mediacentre/factsheets/fs103/en/index.html cited February 2, 2007