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Ann Thorac Surg 2003;76:605-607
© 2003 The Society of Thoracic Surgeons

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Case report

A case of fatal West Nile virus meningoencephalitis associated with receipt of blood transfusions after open heart surgery

^a Department of Infectious Disease, Cleveland, Ohio, USA
^b Department of Cardiothoracic Anesthesia and Critical Care Medicine,, Cleveland, Ohio, USA
^c Department of Cardiothoracic Surgery, Cleveland, Ohio, USA
^d Department of Cardiology, Cleveland, Ohio, USA
^e Department of Clinical Pathology, Cleveland Clinic Foundation, Cleveland, Ohio, USA

Accepted for publication January 26, 2003.

^* Address reprint requests to Dr Gordon, 9500 Euclid Ave, Mailstop S-32, Cleveland, OH 44195, USA
e-mail: gordons{at}ccf.org

	Abstract

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First identified in the United States in 1999, West Nile virus caused approximately 3,500 infections in the late summer and fall of 2002. The virus is predominantly transmitted by mosquitoes, and the risk of infection through blood product transfusion is believed to be low. We present a case of West Nile virus encephalitis transmitted by red blood cell transfusion at the time of coronary artery bypass grafting that resulted in the patient’s death. Individuals undergoing procedures with high blood product transfusion requirements, such as cardiac surgery or organ transplantation, may be at higher risk of this nosocomial infection during epidemics.

	Introduction

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West Nile virus (WNV) is the most recent of the five mosquito-transmitted encephalitides now endemic in the United States [1]. West Nile virus is primarily an avian virus that is spread by mosquitoes to humans (such as horses and several other mammals) serving as dead-end hosts. West Nile virus was first identified in the New World in a sentinel outbreak in New York City in the fall of 1999 resulting in 62 recognized cases and 7 fatalities [2]. During the late summer and fall of 2002, WNV activity increased in the United States, with approximately 3,500 human cases with laboratory evidence of recent WNV infection and 180 associated deaths reported from 42 states and the District of Columbia [3]. Several studies have described the course of infection and subsequent viremia in humans [4]. The incubation period is relatively short (3 to 16 days) and the duration of viremia is roughly 1 to 2 days shorter than the incubation period. Because of the short period of viremia and lack of a carrier state in humans, mosquitoes are unlikely to transmit WNV from person-to-person.

There is a risk of transmission of WNV through blood transfusion, because most WNV-infected individuals have subclinical infections (estimated apparent-to-inapparent case ratio of 1:150) with a short but defined period of viremia. The risk of transfusion-related WNV transmission is presumed to be highest during epidemics, when the prevalence of viremia in the population would be highest. The estimated risk of WNV transmission during the peak of the 1999 epidemic in Queens, New York using mathematical modeling was 2.7 per 10,000 [5].

Concerns about potential transmission of WNV in recipients of blood transfusions were confirmed with the report of WNV infection in an organ donor and 4 transplant recipients in August 2002 [6]. An investigation showed that the organ donor seroconverted for WNV after receipt of blood components from 63 donors. Four recipients (1 heart, 1 liver, and 2 kidney) had WNV encephalitis develop, with 1 fatality. At least 33 additional cases of WNV infection in recipients of blood transfusions in the United States from August 28, 2002 to October 26, 2002 are ongoing [7]. We report a case of fatal WNV infection transmitted through blood transfusions after coronary artery bypass surgery.

A 74-year-old woman with a history of coronary artery bypass grafting in 1996 was admitted to an outside hospital on August 24, 2002 with acute coronary syndrome. She had a history of chronic pulmonary fibrosis treated with prednisone and diabetes mellitus. A diagnostic left heart cardiac catheterization showed an akinetic apex with an ejection fraction of 35%. The patient had severe native vessel disease with patent saphenous vein grafts but high-grade stenosis in the left anterior descending artery and second diagonal not perfused by her grafts. She was subsequently transferred to the Cleveland Clinic and underwent redo-coronary artery bypass graft (saphenous vein graft to right coronary and sequential saphenous vein grafts to diagonal and left anterior descending artery) on September 3, 2002. Her postoperative course was remarkable for thrombocytopenia (2,000/µL with a negative heparin associated antibody). The patient had an oral temperature of 37.6°C develop on the fifth postoperative day, and two sets of blood cultures yielded methicillin-resistant coagulase-negative staphylococci attributed to a central intravenous catheter. Intravenous vancomycin was started and the line was removed, but the patient subsequently had a high fever (39°C) develop, along with generalized weakness and an altered mental status by the fifteenth postoperative day (day 25 of hospitalization). The vancomycin was changed to linezolid (Pharmacia, Norway) because of the concern for drug fever. The fevers eventually resolved, however the encephalopathy progressed and she became unresponsive. A computed tomographic scan of the head without contrast was unremarkable and an electroencephalogram was consistent with a metabolic encephalopathy without epiletiform waves.

A magnetic resonance image of the head showed small patchy foci of hyperintensity in the thalami, each lentiform nucleus, and in the supratentorial white matter and the pons consistent with remote small vessel ischemia. Notably by postoperative day 6, the patient had received a total of 28 units of blood products (12 units of red blood cells and 16 units of platelet concentrate) before the onset of encephalopathy. Because of the possibility of transfusion associated WNV, serum was sent and was positive for WNV-specific immunoglobulin M (8.66, normal < 0.9) and immunoglobulin G antibodies (2.04, normal < 2.0). A lumbar puncture yielded clear cerebrospinal fluid with 2 white blood cells per µL and protein of 76 mg per µL. Cerebrospinal fluid tested positive for WNV-specific immunoglobulin M antibody (6.90, normal < 0.9). Cultures of cerebrospinal fluid were sterile for bacteria and fungi and negative for nucleic acid amplification of herpes simplex virus by polymerase chain reaction. The patient expired on postoperative day 41.

A postmortem examination (limited to the brain) showed the gross brain to be unremarkable, weighing 1,120 g after fixation. Histopathologic examination showed an inflammatory lymphocytic infiltrate of primarily CD3⁺ T-lymphocytes consistent with viral meningoencephalitis.

The Centers for Disease Control and Prevention investigated this case with officials from the American Red Cross. On December 19, 2002, we were notified that one of the blood donors had been implicated as a source of the infection. A retained segment from the unit contained WNV nucleic acid. A follow-up serum sample from the donor contained antibodies to WNV. A unit ofleukocyte-reduced red blood cells from this donor had been transfused to our patient between September 3, 2002 and September 4, 2002.

	Comment

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The extended interval between admission to the hospital and onset of encephalopathy suggested the possibility of nosocomial WNV infection transmitted through blood products, which was confirmed through a subsequent investigation by the Centers for Disease Control and Prevention. At least 33 cases of WNV infections in recipients of blood transfusions in 15 states are being investigated by the Centers for Disease Control and Prevention [7]. At least 7 cases (including ours) have been confirmed with donations that tested positive by polymerase chain reaction or donors that seroconverted after donation. All recipients received components from multiple donors (mean, 42 donors) and 42% (14 cases) underwent surgical procedures of which 50% were coronary artery bypass surgeries.

Reducing the risk of WNV infection from blood transfusions when there is active WNV transmission in the community is an important public health issue. Although prior estimates of the risk are viewed as small (perhaps 1:10,000), subsequent infections may be fatal. In addition, patients undergoing procedures (such as open heart surgery) in which multiple blood product transfusions may be necessary are at higher risk. Screening donor blood for WNV serology would not be an effective strategy, as the period of viremia may antedate appearance of antibodies and immunoglobulin M antibodies against WNV may persist for more than 500 days. Nucleic amplification testing, which is currently used to screen blood for human immunodeficiency virus and hepatitis C virus, is not available and is not recommended for WNV yet.

In lieu of additional information from ongoing studies of WNV transmission by blood products, the American Association of Blood Banks recommends the following [8]:

1. Blood donors in communities with active WNV transmission should be encouraged to report flu-like illnesses associated with fever (> 38.3°C) during the 2 weeks after blood donations.
   
2. On receipt of postdonation information of a suspected WNV infection (flu-like symptoms and fever > 38.3°C), retrieval and quarantine should be made of the extant products collected from 14 days before and 28 days after the onset of illness.
   
3. A donor with a diagnosis of WNV infection should be deferred for 14 days after they have recovered or 28 days from the onset of illness (whichever time period is longer).
   
4. In order to have a blood sample for investigations of suspected WNV transmission by blood products, the blood centers should maintain all retention samples for 90 days or more after the donation date.
   

Clinicians should remain vigilant for the possibility of patients who have WNV infection develop after receiving blood transfusions within the month preceding illness onset in communities where the WNV infection is active.

	References

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1. Petersen L.R., Roehig J.T., Hughes J.M. West Nile virus encephalitis. N Engl J Med 2002;347:1225-1226.[Free Full Text]
2. Asnis D.S., Conetta R., Teixeira A.A., Waldman G., Sampson B.A. The West Nile virus outbreak of 1999 in New York: The Flushing Hospital experience. Clin Inf Dis 2000;30:413-418.[Medline]
3. CDC. West Nile virus activity—United States. MMWR 2002;51:999-1000.
4. Southam C.M., Moore A.E. Induced virus infections in man by the Egypt isolates of West Nile virus. Am J Trop Med Hyg 1954;3:19-50.
5. Biggerstaff B.J., Petersen L.R. Estimated risk of West Nile virus transmission through blood transfusion during an epidemic in Queens, New York City. Transfusion 2002;42:1019-1026.[Medline]
6. CDC. Update investigations of West Nile virus infections in recipients of organ transplantation and blood transfusion. MMWR 2002;51:833-836.[Medline]
7. CDC. Public Health Dispatch. Investigations of West Nile virus infections in recipients of blood transfusions. MMWR 2002;51:973-974.[Medline]
8. Information regarding West Nile virus (www.cdc.gov/od/oc/media/wncount.htm [accessed 11/14/02])

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Nicholas G. Smedira Steven M. Gordon Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Armstrong, W. S. Articles by Gordon, S. M. Search for Related Content PubMed PubMed Citation Articles by Armstrong, W. S. Articles by Gordon, S. M. Related Collections Cardiac - other