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Listeria monocytogenes encephalitis mimicking west nile encephalitis
ISSUES IN INFECTIOUS DISEASE
Listeria monocytogenes encephalitis mimicking West Nile encephalitis Burke A. Cunha, MD,a Alina Filozov, DO,a and Patrick Reme´, MD,b Mineola and Stony Brook, New York
We present a case of a 50-year-old man who presented to Winthrop-University Hospital in the midst of the 2002 West Nile encephalitis (WNE) outbreak with the cardinal clinical findings of WNE, ie, fever, encephalopathy, weakness, and muscle tremors. During the summer of 2002, several cases of aseptic meningitis/viral encephalitis were admitted to our emergency room weekly. In addition, cases of WNE were being admitted at the same time. During this period we had 3 cases of WNE. Our patient presented with the clinical findings of WNE. However, laboratory and radiologic findings suggested the possibility of Listeria monocytogenes encephalitis. The cerebrospinal fluid findings included red blood cells, which, in the absence of a traumatic tap or HSV encephalitis, argue against the diagnosis of WNE but are consistent with L. monocytogenes encephalitis. Computed tomography scan showed communicating hydrocephalus, which also suggests the possibility of L. monocytogenes and argued against the diagnosis of WNE. Clinicians should be vigilant for the mimics of WNE in geographical areas where WNE outbreaks are occurring. (Heart Lung® 2004;33:61-4.)
INTRODUCTION Until recently, West Nile encephalitis (WNE) has been an important arthropod-borne viral cause of encephalitis in Asia, Europe, and Africa. Currently, the epidemiology and clinical features of WNE have been well described before the United States’ experience. In reports from Israel and Romania, WNE has typically been found in patients with fever, headache, myalgias, and encephalopathy. Weakness, rash, generalized adenopathy, and seizures were common in the European and African experience. WNE is said to be the commonest cause of aseptic meningitis/encephalitis in emergency rooms in Cairo. In 2001, WNE was introduced into the United States and spread via migrating birds. The initial epicenter of the outbreak was the New York City area. By 2002, WNE had spread along the eastern seaboard and had extended westward, with From the aInfectious Disease Division, Winthrop-University Hospital, Mineola, New York, and the bState University of New York School of Medicine, Stony Brook, New York. Reprint requests: Burke A. Cunha, MD, Chief, Infectious Disease Division, Winthrop-University Hospital, Mineola, NY 11501. 0147-9563/$30.00 Copyright © 2004 by Elsevier Inc. doi:10.016/j.hrtlng.2003.07.001
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cases appearing in almost all states east of the Rocky Mountains. Because WNE is a newly introduced virus in North America, there is no latent immunity and many deaths have resulted from the outbreaks that have occurred across the United States in 2002. Elderly adults are most frequently affected and have the worst prognosis. The peak occurrence of WNE occurs during the mosquito season and parallels the occurrence of WNE in migrating birds.1–5 During the summer months, viral meningoencephalitis and viral encephalitis are common reasons for admission to the hospital. Most patients are not seriously ill, but some require intensive care and some, particularly with herpes simplex virus 1, (HSV-1) encephalitis have a fatal outcome. The main clinical problem in the summer months is to differentiate common causes of aseptic meningitis, eg, enteroviral aseptic meningitis from HSV-1 aseptic meningitis, meningoencephalitis, or encephalitis. There is considerable clinical overlap in HSV-1 central nervous system infections. The best way to identify HSV-1 encephalitis is by finding the presence of red blood cells in the cerebrospinal fluid (CSF) in advanced cases or by demonstrating a focal temporal lobe focus on electroencephalogram, head
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Cunha, Filozov, and Reme´
Listeria monocytogenes encephalitis mimicking West Nile encephalitis
computed tomography (CT), or magnetic resonance imaging (MRI). The diagnosis of HSV meningoencephalitis infection may be confirmed by HSV-1 PCR of the CSF.3,6 The introduction of WNE into the United States adds another clinical entity to the differential diagnosis of viral meningitis/encephalitis. We present a case of a man admitted during the summer months in the midst of a WNE outbreak superimposed against the usual increased incidence of enteroviral meningitis that occurs during the summer months, and the continuous, non-episodic occurrence of HSV-1 encephalitis. Our patient had the clinical features of WNE, but his encephalitis was caused by L. monocytogenes.
ILLUSTRATIVE CASE The patient is a 75-year-old man who was admitted the hospital with weakness and mental confusion. Weakness was more profound in lower extremities, and he also complained of upper extremity tremors for 2 weeks. Past medical history included pneumonia, coronary artery bypass graft, chronic lymphocytic leukemia, and alcoholic cirrhosis. The patient was penicillin allergic. The physical examination was unremarkable except for a systolic ejection murmur (II/VI), mild hepatomegaly, and a maculopapular truncal rash. Neurologically, he was confused with decreased strength in all extremities and upper extremity tremors. His temperature was 98.4° F, pulse was 100 beats per minute, respiratory rate was 26 respirations per minute, and blood pressure was 100 over 60 mm Hg. Laboratory tests included a white blood cell (WBC) count of 43.6 K per mm3 (PMNs ⫽ 78%, lymphocytes ⫽ 4%, atypical lymphocytes ⫽ 2, monocytes ⫽ 13%, eosinophils ⫽ 2%, basophils ⫽ 1%), hemoglobin/hematocrit ⫽ 14.9 g/dL/44.1%, platelet count ⫽ 180 K per mm; pt/inr/ptt ⫽ 16.8 sec/1.40/36.5 sec, sodium ⫽ 137 mEq per L, potassium ⫽ 4 mEq per L, chloride ⫽ 99 mEq per L, bicarbonate ⫽ 16 mEq per L, blood urea nitrogen ⫽ 50 mg per dL, creatinine ⫽ 3.4 mg per dL, glucose ⫽ 153 mg per dL, calcium ⫽ 9.1 mg per dL, creatinine phosphokinase ⫽ 94 U per L, total protein ⫽ 7.0 g per dL, albumin ⫽ 3.3 g per dL, bilirubin (total) ⫽ 3.6 mg per dL, bilirubin (direct) ⫽ 1.7 mg per dL, SGPT ⫽ 41 U per L, SGOT ⫽ 56 U per L, and the alkaline phosphatase ⫽ 148 U per L. Electrocardiogram obtained showed normal sinus rhythm at 89 beats per minute, left axis deviation, premature ventricular contractions, and tall R wave in V2. Patient had increased vascular markings
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Fig 1. CT scan of head revealing communicating hydrocephalus.
on chest x-ray. CT Scan of abdomen and pelvis was remarkable for gallstones and mild splenomegaly. No dilatation of the intrahepatic biliary tree was noted. CT scan of the head revealed communicating hydrocephalus (Fig 1). CSF analysis revealed red blood cells (RBCs) ⫽ 500 per mm3, WBC ⫽ 756 K per mm3 (PMNs ⫽ 62%, lymphocytes ⫽ 19%, monocytes ⫽ 19%), glucose ⫽ 6 mg per dL, protein ⫽ 386 g per dL, and lactic acid ⫽ 13.6 mg per dL, (Nⱕ 2.2 mg/dL). The CSF Gram stain was negative.
HOSPITAL COURSE On a hospital day 2, the patient’s temperature was 103.8° F with pulse of 80 beats per minute. The patient was agitated, combative, and unable to respond. Vancomycin, 1 g intravenously (IV) q 24 hours, meropenem 1 g (IV) q 12 hours, trimethoprimsulfamethoxazole (TMP-SMX) 320 mg (IV) q 8 hours, and acyclovir 900 mg (IV) q 24 hours, were started empirically pending CSF culture results. Repeat of WBC count was 48.2 K per mm3 and the platelet count was 180 K per mm. Amylase and lipase were
JANUARY/FEBRUARY 2004
HEART & LUNG
Listeria monocytogenes encephalitis mimicking West Nile encephalitis
Cunha, Filozov, and Reme´
Table 1 Clinical features of listeria encephalitis and West Nile encephalitis
Predisposing Factors
Listeria
WNE
Iron overload disorders Cirrhosis Iron overload disorders Steroids
Mosquito bites Organ transplants
⫹ ⫹ ⫹ ⫺ ⫺ ⫺
⫹ ⫹ ⫺ ⫹ ⫹ ⫹
⫹ ⫺ ⫹ ⫺ ⫺
⫹ ⫹ ⫾ ⫾ ⫾
⫺
⫾
⫺ ⫺ ⫺ ⫺
⫾ ⫹ ⫹ ⫾
⫾ ⫹ ⫹ ⫹ ⫹ ⫹ cerebritis
⫺ ⫺ ⫹ ⫺ ⫺ ⫺ hydrocephalus
Symptoms Mental confusion Headache Chills Myalgias/arthralgias Muscle tremors Muscle weakness Signs Fever Relative bradycardia Stiff neck Maculopapular rash Generalized lymphadenopathy Flaccid paralysis Laboratory Abnormalities Leukopenia Thrombocytopenia Lymphopenia Mildly 1SGOT/SGPT CSF Gram stain Culture Pleocytosis Red blood cells Lactic acid (⬎ 6 mg/dL) Glucose Head CT/MRI
SGOT ⫽ serum glutamate oxaloacetate transaminase; SGPT ⫽ serum glutamate pyruvate transaminase.
normal. CSF cultures were negative for bacteria. Blood cultures were positive for gram-positive bacilli. Antimicrobial therapy was discontinued except for TMP-SMX. On hospital day 3, the patient’s temperature remained elevated at 102.4° F, with a pulse of 85 beats per minute and blood pressure 92 over 44 mm Hg. The patient had decreased systolic blood pressure to 70 mm Hg despite IV fluids and pressors. On hospital day 4, the WBC count was 40.7 K per mm3 (PMNs ⫽ 85%, lymphocytes ⫽ 2%, monocytes ⫽ 10%, eosinophils ⫽ 1%), and platelet count was 133 K per mm. The bicarbonate was 18 mEq per L, the blood urea nitrogen was 52 mg per dL, and the creatinine was 3.2 mg per dL.
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Among other tests: ferritin was 5407 ng per mL, albumin was 1.9 g per dL, bilirubin (total) was 1.9 mg per dL, bilirubin (direct) was 0.8 mg per dL, SGPT was 189 U per L, SGOT was 89 U per L, and erythrocyte sedimentation rate was 16 mm per hour. The blood culture isolates from admission were identified as L. monocytogenes. On hospital day 10, the patient developed disseminated intravascular coagulation, became hypotensive, and died.
DISCUSSION In the United States WNE experience, patients typically present acutely with fever, encephalitis,
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Cunha, Filozov, and Reme´
Listeria monocytogenes encephalitis mimicking West Nile encephalitis
muscle weakness, and tremors. Seizures may occur, but rash and generalized adenopathy are unusual. In contrast to enteroviral CNS infections, WNE encephalitis, in addition to mental status changes and fever, may be suggested by the presence of muscle weakness and/or muscle tremors, not a feature of either enteroviral or HSV-1 CNS infections. The electroencephalogram of WNE shows diffuse bilateral slow wave activity, which is also present with other causes of viral encephalitis, eg, Powassan encephalitis. The electroencephalogram is helpful in differentiating HSV-1 encephalitis from WNE encephalitis by the presence or absence of focal findings localized to the temporal lobe, which is characteristic of HSV-1 encephalitis and is not a feature of WNE. Further differentiation may be made by the presence or absence of RBCs in the CSF. RBCs in the CSF are not a feature of enteroviral meningitis but may occur in late or advanced HSV-1 encephalitis. Excluding a traumatic tap, RBCs are not a feature of WNE. A low CSF glucose may occasionally accompany enteroviral or HSV-1 encephalitis but is usually normal in WNE.3,6 L. monocytogenes CNS infections may manifest clinically as meningitis, meningoencephalitis, rhombo-encephalitis, or encephalitis. The clinical presentation of Listeria meningitis is the same as other CNS bacteria causing meningitis, except for the distinguishing presence of CSF RBCs in L. monocytogenes meningitis. Otherwise, the CSF parameters in L. monocytogenes CNS infection are the same as with other CNS bacterial profiles, eg, PMN pleocytosis, decreased glucose, elevated protein, elevated lactic acid levels. CT and MRI scans in bacterial meningitis are usually unremarkable, but noncommunicating hydrocephaly is frequent with L. monocytogenes, and may be a clue to its presence.5–11 When L. monocytogenes presents as encephalitis, it most closely mimics HSV-1 encephalitis. Both often have CSF RBCs, CSF PMN pleocytosis, decreased glucose, increased protein, and a negative CSF Gram stain. The CSF Gram stain is negative in approximately 50% of cases, but CSF cultures are positive in approximately 100% of case (Table 1).12–17 The preferred antimicrobial therapy of Listeria CNS infections is ampicillin or TMP-SMX. Alternately, choramphenicol may be used.18 –22 WNE is rapidly spreading across the United States. Presently, with encephalitis, it is most easily confused with HSV-1 encephalitis, but other etiologies of encephalitis should be included in the differential diagnosis, eg, Powassan encephalitis, western encephalitis, eastern encephalitis, St. Louis
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encephalitis, and tickborne encephalidities. The case presented was initially thought to be WNE because it occurred during a WNE outbreak and had many clinical features in common with WNE. Clinicians should be vigilant and aware of the many mimics of WNE. REFERENCES 1. Marfin AA, Gubler DJ. West Nile encephalitis. An emerging disease in the United States. Clin Infect Dis 2001;33:1713-9. 2. Centers for Disease Control and Prevention. West Nile Virus activity—United States, 2001. MMWR Morb Mortal Wkly Rep 2002;23:497-501. 3. Cunha BA. West Nile encephalitis. Infect Dis Practice 1999; 23:85-90. 4. Asnis DS, Conetta R, Teixeira AA, et al. The West Nile Virus outbreak of 1999 in New York. The Flushing Hospital experience. Clin Infect Dis 2000;30:413-8. 5. Louria DB, Blevins A, Armstrong D. Listeria infections. Ann NY Acad Sci 1970;174:545-51. 6. Lorber B. Listeriosis. Infect Dis Practice 2001;25:45-8. 7. Mylonakis E, Hohmann EL, Calderwood SB. Central nervous system infection with Listeria monocytogenes. 33 years’ experience at a general hospital and review of 776 episodes from the literature. Medicine (Baltimore) 1998;77:313-36. 8. Hansen PB, Jensen TH, Lykkegaard S, Kristensen HS. Listeria monocytogenes meningitis in adults. Sixteen consecutive cases 1973-1982. Scand J Infect Dis 1987;19:55-60. 9. Iwarson S, Lidin-Janson G, Svensson R. Listeric meningitis in noncompromised host. Infection 1977;5:204-6. 10. Bouvet E, Suter F, Gibert C, Witchitz JL, Basin C, Vachon F. Severe meningitis due to Listeria monocytogenes. A review of 40 cases in adults. Scand J Infect Dis 1982;14:267-70. 11. Buchner LH, Schneierson S. Clinical and laboratory aspects of Listeria monocytogenes infections. With a report of ten cases. Am J Med 1968;45:904-21. 12. Armstrong DW, Fung PC. Brainstem encephalitis (rhombencephalitis) due to Listeria monocytogenes. Case report and review. Clin Infect Dis 1993;16:689-702. 13. Uldry PA, Kuntzer T, Bogousslavsky J. Early symptoms and outcome of Listeria monocytogenes rhombencephalitis. 14 adult cases. J Neurol 1993;240:235-42. 14. Taege AJ. Listeriosis. Recognizing it, treating it, preventing it. Cleve Clin J Med 1999;66:375-80. 15. Heck AF, Hameroff SB, Hornick RB. Chronic Listeria monocytogenes meningitis and normotensive hydrocephalus. Case report and review. Neurology 1971;21:263-70. 16. Marrie TJ, Riding M, Grant B. Computed tomographic scanning in Listeria monocytogenes meningitis. Clin Invest Med 1984; 7:355-59. 17. Gholizadeh Y, Yuvin M, Beretti JL, Berche P, Gaillard JL. Culture-negative listeriosis of the central nervous system diagnosed by detection of antibodies to listeriolysin O [letter]. Eur J Clin Microbiol Infect Dis 1997;16:176-8. 18. Levitz RE, Quintiliani R. Trimethoprim-sulfamethoxazole for bacterial meningitis. Ann Intern Med 1984;100:881-90. 19. Jacquette G, Dennehy PH. Trimethoprim-sulfamethoxazole in Listeria monocytogenes meningitis. Ann Intern Med 1985;102: 866-7. 20. Friedrich LV, White RL, Reboli AC. Pharmacodynamics of trimethoprim-sulfamethoxazole in Listeria meningitis. A case report. Pharmacotherapy 1990;10:301-4. 21. Hof H, Nichterlein T, Kretschmar M. Management of listeriosis. Clin Microbiol Rev 1997;10:345-57. 22. Gunther G, Philipson A. Oral trimethoprim as follow up treatment of meningitis caused by Listeria monocytogenes. Rev Infect Dis 1988;10:53-5.
JANUARY/FEBRUARY 2004
HEART & LUNG
Listeria monocytogenes encephalitis mimicking West Nile encephalitis Burke A. Cunha, MD,a Alina Filozov, DO,a and Patrick Reme´, MD,b Mineola and Stony Brook, New York
We present a case of a 50-year-old man who presented to Winthrop-University Hospital in the midst of the 2002 West Nile encephalitis (WNE) outbreak with the cardinal clinical findings of WNE, ie, fever, encephalopathy, weakness, and muscle tremors. During the summer of 2002, several cases of aseptic meningitis/viral encephalitis were admitted to our emergency room weekly. In addition, cases of WNE were being admitted at the same time. During this period we had 3 cases of WNE. Our patient presented with the clinical findings of WNE. However, laboratory and radiologic findings suggested the possibility of Listeria monocytogenes encephalitis. The cerebrospinal fluid findings included red blood cells, which, in the absence of a traumatic tap or HSV encephalitis, argue against the diagnosis of WNE but are consistent with L. monocytogenes encephalitis. Computed tomography scan showed communicating hydrocephalus, which also suggests the possibility of L. monocytogenes and argued against the diagnosis of WNE. Clinicians should be vigilant for the mimics of WNE in geographical areas where WNE outbreaks are occurring. (Heart Lung® 2004;33:61-4.)
INTRODUCTION Until recently, West Nile encephalitis (WNE) has been an important arthropod-borne viral cause of encephalitis in Asia, Europe, and Africa. Currently, the epidemiology and clinical features of WNE have been well described before the United States’ experience. In reports from Israel and Romania, WNE has typically been found in patients with fever, headache, myalgias, and encephalopathy. Weakness, rash, generalized adenopathy, and seizures were common in the European and African experience. WNE is said to be the commonest cause of aseptic meningitis/encephalitis in emergency rooms in Cairo. In 2001, WNE was introduced into the United States and spread via migrating birds. The initial epicenter of the outbreak was the New York City area. By 2002, WNE had spread along the eastern seaboard and had extended westward, with From the aInfectious Disease Division, Winthrop-University Hospital, Mineola, New York, and the bState University of New York School of Medicine, Stony Brook, New York. Reprint requests: Burke A. Cunha, MD, Chief, Infectious Disease Division, Winthrop-University Hospital, Mineola, NY 11501. 0147-9563/$30.00 Copyright © 2004 by Elsevier Inc. doi:10.016/j.hrtlng.2003.07.001
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cases appearing in almost all states east of the Rocky Mountains. Because WNE is a newly introduced virus in North America, there is no latent immunity and many deaths have resulted from the outbreaks that have occurred across the United States in 2002. Elderly adults are most frequently affected and have the worst prognosis. The peak occurrence of WNE occurs during the mosquito season and parallels the occurrence of WNE in migrating birds.1–5 During the summer months, viral meningoencephalitis and viral encephalitis are common reasons for admission to the hospital. Most patients are not seriously ill, but some require intensive care and some, particularly with herpes simplex virus 1, (HSV-1) encephalitis have a fatal outcome. The main clinical problem in the summer months is to differentiate common causes of aseptic meningitis, eg, enteroviral aseptic meningitis from HSV-1 aseptic meningitis, meningoencephalitis, or encephalitis. There is considerable clinical overlap in HSV-1 central nervous system infections. The best way to identify HSV-1 encephalitis is by finding the presence of red blood cells in the cerebrospinal fluid (CSF) in advanced cases or by demonstrating a focal temporal lobe focus on electroencephalogram, head
www.heartandlung.org
61
Cunha, Filozov, and Reme´
Listeria monocytogenes encephalitis mimicking West Nile encephalitis
computed tomography (CT), or magnetic resonance imaging (MRI). The diagnosis of HSV meningoencephalitis infection may be confirmed by HSV-1 PCR of the CSF.3,6 The introduction of WNE into the United States adds another clinical entity to the differential diagnosis of viral meningitis/encephalitis. We present a case of a man admitted during the summer months in the midst of a WNE outbreak superimposed against the usual increased incidence of enteroviral meningitis that occurs during the summer months, and the continuous, non-episodic occurrence of HSV-1 encephalitis. Our patient had the clinical features of WNE, but his encephalitis was caused by L. monocytogenes.
ILLUSTRATIVE CASE The patient is a 75-year-old man who was admitted the hospital with weakness and mental confusion. Weakness was more profound in lower extremities, and he also complained of upper extremity tremors for 2 weeks. Past medical history included pneumonia, coronary artery bypass graft, chronic lymphocytic leukemia, and alcoholic cirrhosis. The patient was penicillin allergic. The physical examination was unremarkable except for a systolic ejection murmur (II/VI), mild hepatomegaly, and a maculopapular truncal rash. Neurologically, he was confused with decreased strength in all extremities and upper extremity tremors. His temperature was 98.4° F, pulse was 100 beats per minute, respiratory rate was 26 respirations per minute, and blood pressure was 100 over 60 mm Hg. Laboratory tests included a white blood cell (WBC) count of 43.6 K per mm3 (PMNs ⫽ 78%, lymphocytes ⫽ 4%, atypical lymphocytes ⫽ 2, monocytes ⫽ 13%, eosinophils ⫽ 2%, basophils ⫽ 1%), hemoglobin/hematocrit ⫽ 14.9 g/dL/44.1%, platelet count ⫽ 180 K per mm; pt/inr/ptt ⫽ 16.8 sec/1.40/36.5 sec, sodium ⫽ 137 mEq per L, potassium ⫽ 4 mEq per L, chloride ⫽ 99 mEq per L, bicarbonate ⫽ 16 mEq per L, blood urea nitrogen ⫽ 50 mg per dL, creatinine ⫽ 3.4 mg per dL, glucose ⫽ 153 mg per dL, calcium ⫽ 9.1 mg per dL, creatinine phosphokinase ⫽ 94 U per L, total protein ⫽ 7.0 g per dL, albumin ⫽ 3.3 g per dL, bilirubin (total) ⫽ 3.6 mg per dL, bilirubin (direct) ⫽ 1.7 mg per dL, SGPT ⫽ 41 U per L, SGOT ⫽ 56 U per L, and the alkaline phosphatase ⫽ 148 U per L. Electrocardiogram obtained showed normal sinus rhythm at 89 beats per minute, left axis deviation, premature ventricular contractions, and tall R wave in V2. Patient had increased vascular markings
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Fig 1. CT scan of head revealing communicating hydrocephalus.
on chest x-ray. CT Scan of abdomen and pelvis was remarkable for gallstones and mild splenomegaly. No dilatation of the intrahepatic biliary tree was noted. CT scan of the head revealed communicating hydrocephalus (Fig 1). CSF analysis revealed red blood cells (RBCs) ⫽ 500 per mm3, WBC ⫽ 756 K per mm3 (PMNs ⫽ 62%, lymphocytes ⫽ 19%, monocytes ⫽ 19%), glucose ⫽ 6 mg per dL, protein ⫽ 386 g per dL, and lactic acid ⫽ 13.6 mg per dL, (Nⱕ 2.2 mg/dL). The CSF Gram stain was negative.
HOSPITAL COURSE On a hospital day 2, the patient’s temperature was 103.8° F with pulse of 80 beats per minute. The patient was agitated, combative, and unable to respond. Vancomycin, 1 g intravenously (IV) q 24 hours, meropenem 1 g (IV) q 12 hours, trimethoprimsulfamethoxazole (TMP-SMX) 320 mg (IV) q 8 hours, and acyclovir 900 mg (IV) q 24 hours, were started empirically pending CSF culture results. Repeat of WBC count was 48.2 K per mm3 and the platelet count was 180 K per mm. Amylase and lipase were
JANUARY/FEBRUARY 2004
HEART & LUNG
Listeria monocytogenes encephalitis mimicking West Nile encephalitis
Cunha, Filozov, and Reme´
Table 1 Clinical features of listeria encephalitis and West Nile encephalitis
Predisposing Factors
Listeria
WNE
Iron overload disorders Cirrhosis Iron overload disorders Steroids
Mosquito bites Organ transplants
⫹ ⫹ ⫹ ⫺ ⫺ ⫺
⫹ ⫹ ⫺ ⫹ ⫹ ⫹
⫹ ⫺ ⫹ ⫺ ⫺
⫹ ⫹ ⫾ ⫾ ⫾
⫺
⫾
⫺ ⫺ ⫺ ⫺
⫾ ⫹ ⫹ ⫾
⫾ ⫹ ⫹ ⫹ ⫹ ⫹ cerebritis
⫺ ⫺ ⫹ ⫺ ⫺ ⫺ hydrocephalus
Symptoms Mental confusion Headache Chills Myalgias/arthralgias Muscle tremors Muscle weakness Signs Fever Relative bradycardia Stiff neck Maculopapular rash Generalized lymphadenopathy Flaccid paralysis Laboratory Abnormalities Leukopenia Thrombocytopenia Lymphopenia Mildly 1SGOT/SGPT CSF Gram stain Culture Pleocytosis Red blood cells Lactic acid (⬎ 6 mg/dL) Glucose Head CT/MRI
SGOT ⫽ serum glutamate oxaloacetate transaminase; SGPT ⫽ serum glutamate pyruvate transaminase.
normal. CSF cultures were negative for bacteria. Blood cultures were positive for gram-positive bacilli. Antimicrobial therapy was discontinued except for TMP-SMX. On hospital day 3, the patient’s temperature remained elevated at 102.4° F, with a pulse of 85 beats per minute and blood pressure 92 over 44 mm Hg. The patient had decreased systolic blood pressure to 70 mm Hg despite IV fluids and pressors. On hospital day 4, the WBC count was 40.7 K per mm3 (PMNs ⫽ 85%, lymphocytes ⫽ 2%, monocytes ⫽ 10%, eosinophils ⫽ 1%), and platelet count was 133 K per mm. The bicarbonate was 18 mEq per L, the blood urea nitrogen was 52 mg per dL, and the creatinine was 3.2 mg per dL.
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Among other tests: ferritin was 5407 ng per mL, albumin was 1.9 g per dL, bilirubin (total) was 1.9 mg per dL, bilirubin (direct) was 0.8 mg per dL, SGPT was 189 U per L, SGOT was 89 U per L, and erythrocyte sedimentation rate was 16 mm per hour. The blood culture isolates from admission were identified as L. monocytogenes. On hospital day 10, the patient developed disseminated intravascular coagulation, became hypotensive, and died.
DISCUSSION In the United States WNE experience, patients typically present acutely with fever, encephalitis,
www.heartandlung.org
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Cunha, Filozov, and Reme´
Listeria monocytogenes encephalitis mimicking West Nile encephalitis
muscle weakness, and tremors. Seizures may occur, but rash and generalized adenopathy are unusual. In contrast to enteroviral CNS infections, WNE encephalitis, in addition to mental status changes and fever, may be suggested by the presence of muscle weakness and/or muscle tremors, not a feature of either enteroviral or HSV-1 CNS infections. The electroencephalogram of WNE shows diffuse bilateral slow wave activity, which is also present with other causes of viral encephalitis, eg, Powassan encephalitis. The electroencephalogram is helpful in differentiating HSV-1 encephalitis from WNE encephalitis by the presence or absence of focal findings localized to the temporal lobe, which is characteristic of HSV-1 encephalitis and is not a feature of WNE. Further differentiation may be made by the presence or absence of RBCs in the CSF. RBCs in the CSF are not a feature of enteroviral meningitis but may occur in late or advanced HSV-1 encephalitis. Excluding a traumatic tap, RBCs are not a feature of WNE. A low CSF glucose may occasionally accompany enteroviral or HSV-1 encephalitis but is usually normal in WNE.3,6 L. monocytogenes CNS infections may manifest clinically as meningitis, meningoencephalitis, rhombo-encephalitis, or encephalitis. The clinical presentation of Listeria meningitis is the same as other CNS bacteria causing meningitis, except for the distinguishing presence of CSF RBCs in L. monocytogenes meningitis. Otherwise, the CSF parameters in L. monocytogenes CNS infection are the same as with other CNS bacterial profiles, eg, PMN pleocytosis, decreased glucose, elevated protein, elevated lactic acid levels. CT and MRI scans in bacterial meningitis are usually unremarkable, but noncommunicating hydrocephaly is frequent with L. monocytogenes, and may be a clue to its presence.5–11 When L. monocytogenes presents as encephalitis, it most closely mimics HSV-1 encephalitis. Both often have CSF RBCs, CSF PMN pleocytosis, decreased glucose, increased protein, and a negative CSF Gram stain. The CSF Gram stain is negative in approximately 50% of cases, but CSF cultures are positive in approximately 100% of case (Table 1).12–17 The preferred antimicrobial therapy of Listeria CNS infections is ampicillin or TMP-SMX. Alternately, choramphenicol may be used.18 –22 WNE is rapidly spreading across the United States. Presently, with encephalitis, it is most easily confused with HSV-1 encephalitis, but other etiologies of encephalitis should be included in the differential diagnosis, eg, Powassan encephalitis, western encephalitis, eastern encephalitis, St. Louis
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encephalitis, and tickborne encephalidities. The case presented was initially thought to be WNE because it occurred during a WNE outbreak and had many clinical features in common with WNE. Clinicians should be vigilant and aware of the many mimics of WNE. REFERENCES 1. Marfin AA, Gubler DJ. West Nile encephalitis. An emerging disease in the United States. Clin Infect Dis 2001;33:1713-9. 2. Centers for Disease Control and Prevention. West Nile Virus activity—United States, 2001. MMWR Morb Mortal Wkly Rep 2002;23:497-501. 3. Cunha BA. West Nile encephalitis. Infect Dis Practice 1999; 23:85-90. 4. Asnis DS, Conetta R, Teixeira AA, et al. The West Nile Virus outbreak of 1999 in New York. The Flushing Hospital experience. Clin Infect Dis 2000;30:413-8. 5. Louria DB, Blevins A, Armstrong D. Listeria infections. Ann NY Acad Sci 1970;174:545-51. 6. Lorber B. Listeriosis. Infect Dis Practice 2001;25:45-8. 7. Mylonakis E, Hohmann EL, Calderwood SB. Central nervous system infection with Listeria monocytogenes. 33 years’ experience at a general hospital and review of 776 episodes from the literature. Medicine (Baltimore) 1998;77:313-36. 8. Hansen PB, Jensen TH, Lykkegaard S, Kristensen HS. Listeria monocytogenes meningitis in adults. Sixteen consecutive cases 1973-1982. Scand J Infect Dis 1987;19:55-60. 9. Iwarson S, Lidin-Janson G, Svensson R. Listeric meningitis in noncompromised host. Infection 1977;5:204-6. 10. Bouvet E, Suter F, Gibert C, Witchitz JL, Basin C, Vachon F. Severe meningitis due to Listeria monocytogenes. A review of 40 cases in adults. Scand J Infect Dis 1982;14:267-70. 11. Buchner LH, Schneierson S. Clinical and laboratory aspects of Listeria monocytogenes infections. With a report of ten cases. Am J Med 1968;45:904-21. 12. Armstrong DW, Fung PC. Brainstem encephalitis (rhombencephalitis) due to Listeria monocytogenes. Case report and review. Clin Infect Dis 1993;16:689-702. 13. Uldry PA, Kuntzer T, Bogousslavsky J. Early symptoms and outcome of Listeria monocytogenes rhombencephalitis. 14 adult cases. J Neurol 1993;240:235-42. 14. Taege AJ. Listeriosis. Recognizing it, treating it, preventing it. Cleve Clin J Med 1999;66:375-80. 15. Heck AF, Hameroff SB, Hornick RB. Chronic Listeria monocytogenes meningitis and normotensive hydrocephalus. Case report and review. Neurology 1971;21:263-70. 16. Marrie TJ, Riding M, Grant B. Computed tomographic scanning in Listeria monocytogenes meningitis. Clin Invest Med 1984; 7:355-59. 17. Gholizadeh Y, Yuvin M, Beretti JL, Berche P, Gaillard JL. Culture-negative listeriosis of the central nervous system diagnosed by detection of antibodies to listeriolysin O [letter]. Eur J Clin Microbiol Infect Dis 1997;16:176-8. 18. Levitz RE, Quintiliani R. Trimethoprim-sulfamethoxazole for bacterial meningitis. Ann Intern Med 1984;100:881-90. 19. Jacquette G, Dennehy PH. Trimethoprim-sulfamethoxazole in Listeria monocytogenes meningitis. Ann Intern Med 1985;102: 866-7. 20. Friedrich LV, White RL, Reboli AC. Pharmacodynamics of trimethoprim-sulfamethoxazole in Listeria meningitis. A case report. Pharmacotherapy 1990;10:301-4. 21. Hof H, Nichterlein T, Kretschmar M. Management of listeriosis. Clin Microbiol Rev 1997;10:345-57. 22. Gunther G, Philipson A. Oral trimethoprim as follow up treatment of meningitis caused by Listeria monocytogenes. Rev Infect Dis 1988;10:53-5.
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