Infective Endocarditis Caused by Viridans Streptococci

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Case Study 1: Infective endocarditis caused by viridans streptococci

Case Study 2: Haemorrhagic fever caused by Ebolavirus

Case Study 1

Subject is a 48-year-old man with a history of mitral valve regurgitation who presents with a 10-day history of fatigue, fever and general malaise. Some reddish lesions are noted on his palm, which he has never noticed before. He denies any cough, but has mild new shortness of breath with exertion and with lying down flat at night in bed.

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He is generally in good health except for a root 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 best heard at the left sternal border with radiation over to the axilla. Lungs are clear and abdominal examination is normal. Skin examination is significant for several 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; blood cultures grew out gram-positive cocci in chains that are alpha haemolytic on horse blood agar.

Evidence for Diagnosis

Mitral valve regurgitation would account for the fatigue, and also the shortness of breath in the patient, however 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 (O’Connor, 2002), and the patient’s history of mitral valve regurgitation, along with a recent history of root canal work confirm that this is a likely diagnosis. The lungs and abdomen of the patient are clear, as would be expected in a case of endocarditis, however examination of the heart sounds displayed a clear murmer. The patient’s blood results showed clear signs of infection, with leukocytosis and elevated neutrophil count. The bacteria cultured from the patient’s 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 diagnosis very likely.

Further Testing Required

While 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 tool for diagnosis of infective endocarditis, this patient would be classified as having only possible infective endocarditis. As they display some of the necessary pathologic and clinical criteria, they would need further tests to determine if it was definitely infective endocarditis (Li et al., 2000). The Duke Criteria was developed 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 (Bayer et al., 1994)(Cecchi et al., 1997)(Hoen et al., 1995) The criteria have been used since, though there have been studies done into improving the criteria further. According to these criteria, the patient’s 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 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 streptococci, as Streptococcus pneumonia is more commonly associated with bacterial pneumonia or meningitis, the two can be differentiated quite simply by testing 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 result of streptococcal infection

Microbiology

Many 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 found resident in abundance in the mouth, where they are usually commensal, or cause only mild infections; once in the blood stream, these usually passive bacteria can become pathogenic, and lead 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 (O’Connor, 2002). Those valves damaged by rheumatic fever are particularly prone to infection (Heritage, Evans and Killington, 1999, p.185).

Symptoms

The physical symptoms suffered by the patient are a result of the body’s 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 (O’Connor, 2002).

Prophylaxis

Any 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 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 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.

Treatment

A 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 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 always successful, this offers an improved prognosis for those where other treatment is unsuccessful (Moon et al., 1997).

Prognosis

If left untreated, infective endocarditis is always fatal, as the destruction of a valve will prevent the heart from working. Even if treated, the disease 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 4

A 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 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 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, yellow fever, Crimean-Congo haemorrhagic fever, Marburg virus, Rift Valley fever, Lassa fever, and Hantavirus are all negative.

Evidence for Diagnosis

The 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 patient’s 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 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, 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 Required

While virus isolation, transmission electron microscopy, immunohistochemistry, reverse transcription-PCR, antigen capture ELISA, and IgG or IgM 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 Control 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.

Ebolavirus

Aetiology

Ebola 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 natural 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 suggestion 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 population.

Epidemiology

The disease has appeared sporadically since its initial recognition in 1976, and has occurred only in specific geographical areas as per the names 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 extensive 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 ability 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).

Symptoms

The World Health Organisation (2004) lists the main symptoms of the Ebolavirus 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.

Pathogenesis

The pathogenesis of Ebolavirus is currently very hard to study, due to the rarity 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).

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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 intravascular 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 Treatment

Some 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).

Prognosis

The 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.

References

Bayer 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 Journal of Medicine, 96 (3), pp.220-2

Brooks G.F., Butel J.S. and Morse S.A. (2004) Medical Microbiology23rd Edition. McGraw-Hill, p.197

CDC (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, 2007]

Cecchi E., Parrini I., Chinaglia A., Pomari F., Brusasco G., Bobbio 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. 1149-56

Dowell 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 Infectious Disease, 179 Suppl. 1, pp. S87-S91

Durack 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. 200-9

Elliott M., Hastings U., Desselberger R. and Reid G. (1997) Lecture Notes on Medical Microbiology Oxford, UK: Blackwell Publishing, pp.30-1

Formenty P., Hatz C., Le Guenno B., Stoll A., Rogenmoser P. and Widmer A. (1999) Human infection due to Ebola virus, subtype Cote d’Ivoire: Clinical and biologic presentation. Journal of Infectious Diease, 179 Suppl. 1, pp.S48-S53

Heeney J.L. (2006) Zoonotic viral diseases and the frontier of early diagnosis, control and prevention. Journal of Internal Medicine, 260, pp. 399-408

Hensley 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 – 772

Heritage J., Evans E.G.V. and Killington R.A. (1999) Microbiology in Action. Cambridge, UK: Cambridge University Press, p. 185

Hoen 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. 905-9

Johnson 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. 7283

Johnson 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. 227-236

Karth G.D. [et al.] (2002) Complicated infective endocarditis necessitating ICU admission clinical course and prognosis. Critical Care, 6 (2), pp. 149 – 154

Kurosaki 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.633-638

Mahanty S. and Bray M. (2004) Pathogenesis of filoviral haemorrhagic fevers. The Lancet, 4 (8) pp. 487-498

Moon M.R., Stinson E.B. and Miller D.C. (1997) Surgical treatment of endocarditis. Progress in Cardiovascular Diease, 40 (3) pp. 239-64

O’Connor D. (2002) Pathology. Elsevier Health Sciences

Peters 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 Group 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. 4330-4341

WHO (2005) World Health Organisation – Ebola Factsheet [Online]available at: http://www.who.int/mediacentre/factsheets/fs103/en/index.html [cited February 2, 2007]

Case Study 1: Infective endocarditis caused by viridans streptococci

Case Study 2: Haemorrhagic fever caused by Ebolavirus

Case Study 1

Subject is a 48-year-old man with a history of mitral valve regurgitation who presents with a 10-day history of fatigue, fever and general malaise. Some reddish lesions are noted on his palm, which he has never noticed before. He denies any cough, but has mild new shortness of breath with exertion and with lying down flat at night in bed.

He is generally in good health except for a root 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 best heard at the left sternal border with radiation over to the axilla. Lungs are clear and abdominal examination is normal. Skin examination is significant for several 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; blood cultures grew out gram-positive cocci in chains that are alpha haemolytic on horse blood agar.

Evidence for Diagnosis

Mitral valve regurgitation would account for the fatigue, and also the shortness of breath in the patient, however 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 (O’Connor, 2002), and the patient’s history of mitral valve regurgitation, along with a recent history of root canal work confirm that this is a likely diagnosis. The lungs and abdomen of the patient are clear, as would be expected in a case of endocarditis, however examination of the heart sounds displayed a clear murmer. The patient’s blood results showed clear signs of infection, with leukocytosis and elevated neutrophil count. The bacteria cultured from the patient’s 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 diagnosis very likely.

Further Testing Required

While 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 tool for diagnosis of infective endocarditis, this patient would be classified as having only possible infective endocarditis. As they display some of the necessary pathologic and clinical criteria, they would need further tests to determine if it was definitely infective endocarditis (Li et al., 2000). The Duke Criteria was developed 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 (Bayer et al., 1994)(Cecchi et al., 1997)(Hoen et al., 1995) The criteria have been used since, though there have been studies done into improving the criteria further. According to these criteria, the patient’s 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 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 streptococci, as Streptococcus pneumonia is more commonly associated with bacterial pneumonia or meningitis, the two can be differentiated quite simply by testing 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 result of streptococcal infection

Microbiology

Many 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 found resident in abundance in the mouth, where they are usually commensal, or cause only mild infections; once in the blood stream, these usually passive bacteria can become pathogenic, and lead 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 (O’Connor, 2002). Those valves damaged by rheumatic fever are particularly prone to infection (Heritage, Evans and Killington, 1999, p.185).

Symptoms

The physical symptoms suffered by the patient are a result of the body’s 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 (O’Connor, 2002).

Prophylaxis

Any 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 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 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.

Treatment

A 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 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 always successful, this offers an improved prognosis for those where other treatment is unsuccessful (Moon et al., 1997).

Prognosis

If left untreated, infective endocarditis is always fatal, as the destruction of a valve will prevent the heart from working. Even if treated, the disease 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 4

A 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 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 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, yellow fever, Crimean-Congo haemorrhagic fever, Marburg virus, Rift Valley fever, Lassa fever, and Hantavirus are all negative.

Evidence for Diagnosis

The 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 patient’s 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 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, 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 Required

While virus isolation, transmission electron microscopy, immunohistochemistry, reverse transcription-PCR, antigen capture ELISA, and IgG or IgM 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 Control 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.

Ebolavirus

Aetiology

Ebola 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 natural 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 suggestion 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 population.

Epidemiology

The disease has appeared sporadically since its initial recognition in 1976, and has occurred only in specific geographical areas as per the names 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 extensive 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 ability 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).

Symptoms

The World Health Organisation (2004) lists the main symptoms of the Ebolavirus 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.

Pathogenesis

The pathogenesis of Ebolavirus is currently very hard to study, due to the rarity 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 intravascular 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 Treatment

Some 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).

Prognosis

The 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.

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