A First Clinical Case Report of West-Nile Viral Meningoencephalitis Complicated with Acute Pancreatitis in North America
Received Date: Dec 02, 2015 / Accepted Date: Feb 19, 2016 / Published Date: Feb 27, 2016
Most affected humans with west-nile virus (WNV), a mosquito-borne virus of the flaviviridae family, remain asymptomatic, while a minority may develop neurological manifestation such as meningitis, encephalitis or a flaccid paralysis. Gastrointestinal symptoms such as anorexia and abdominal pain are less common, whereas full blown symptomatic acute pancreatitis has only been described twice in the literature. These cases occurred in the Netherlands and in Israel where WNV is fairly endemic. We report the first clinical case in North America of a previously healthy 52 year old man who developed full blown WNV meningo-encephalitis with concurrent acute pancreatitis. Acute WN viral meningo-encephalitis was confirmed by a lumbar puncture, while other causes of meningitis/encephalitis were excluded. Acute WNV pancreatitis was diagnosed clinically as well as by abnormal serological markers including elevated amylase and lipase levels. The patient was treated conservatively, and his symptoms gradually improved until full recovery, requiring a total of three weeks from onset. WNV and its complications are reviewed, in addition to a description of prior cases of pancreatitis associated with WNV infection.
Keywords: West Nile virus; Infection; Meningitis; Encephalitis; Meningoencephalitis; Acute pancreatitis; Mosquitos
WNV: West-Nile Virus; CSF: Cerebrospinal Fluid; CBC: Complete Blood Count; NPO: Nothing Per Month; CT: Computed Tomography
WNV is a mosquito-borne virus of the flaviviridae family. It is indigenous to Africa, Asia, Europe and Australia , and has been associated with several outbreaks in Israel [2,3]. WNV was virtually unknown to North America until 1999, when it made a first appearance during an epidemic of meningo-encephalitis in Queens, New York, NY . From the period between 1999 and 2004, there have then been over 7,000 reported cases of neuro-invasive WNV induced encephalitis in the United States . The neurological manifestations of WNV infection can range from meningitis, encephalitis and cranial nerve dysfunction to acute flaccid paralysis and motor neuron disease [5-10]. Most cases of WNV infections are asymptomatic. The incubation period is typically 2 to 14 days [11,12]. There are no specific symptoms that typify WNV infections. Clinically, they may present with symptoms similar to aseptic viral meningitis, usually with fever, headache, and other non-specific symptoms. These typically carry a low associated mortality . Some patients may present with a more abrupt onset of encephalitis with altered mental status, vomiting, severe headaches, accompanied by a high grade fever. In about 15% of cases, cerebral dysfunction may progress to coma, with accompanying abnormalities such as diffuse muscle weakness, flaccid paralysis, and respiratory failure [13-15].
The diagnosis of WNV infection is made by obtaining serum and CSF antibodies. False positive serological results may occur in patients who have recently been vaccinated against yellow fever, Japanese encephalitis, or those who had recently been affected with dengue or St-Louis encephalitis. Rarely, WNV has been isolated from other solid organs such as the liver, spleen, lungs and pancreas . Clinical management of WNV infections is generally supportive. All patients with suspected WNV meningitis or meningo-encephalitis should be admitted to an inpatient hospital setting for further observation and supportive care, while ruling out other CNS infection that may be subject to more directed therapy . In this report, we describe a previously healthy man with WNV meningoencephalitis and concurrent acute pancreatitis. To the best of our knowledge, this is the first described case of WNV meningo-encephalitis with concurrent acute clinical and chemical pancreatitis in North America.
A 52 year old man with no prior medical history presented to our center with headache, fever, lethargy and general malaise of about a one-week duration. He denied recent contact with sick individuals, had not sought medical attention, and was not on any home medications. He denied alcohol consumption, smoking and illicit drug use. He also denied any awareness of being recently bitten by arthropods, ticks or animals.
On admission, he was noted to be febrile, lethargic and in moderate distress secondary to abdominal pain (Table 1). His head, eyes, ears, nose, throat, neck, pulmonary and cardiac examinations were unremarkable. His abdominal exam was significant for moderate yet poorly localized tenderness throughout his abdomen, which he rated as 7/10, along with hypoactive bowel sounds and mild guarding without evidence of rebound. His liver and spleen were not palpable.
|Date:||Day 1||Day 6|
|WBC||4.21k (range: 3.2K-10k)||4.45|
|Platelet||327 (range: 150K-450k)||190|
|Total bilirubin||0.8 (range 0.4 mg/dL -1.5 mg/dL)||0.5|
|AST||38 (range 15 U/L -41 U/L)||55|
|ALT||20 (range 14 U/L -54 U/L)||58|
|Alkaline Phosphatase||65 (range 24 U/L -110 U/L)||59|
|Lipase||693 (range 17 U/L -50 U/L)||560|
|Amylase||499 (range 15 U/L -50 U/L)||227|
|Triglyceride||161 (range <150mg/dL)||66|
|Range: <40 mg/dL LOW|
|≥ 60 mg/dL High (Negative Risk Factor)|
|100 mg/dL-129 mg/dL Near Optimal/Above Optimal|
|130 mg/dL-159 mg/dL Borderline High|
|160 mg/dL-189 mg/dL High|
|≥ 190 mg/dL Very high)|
|Calcium (calculated)||10 (range: 8.7 mg/dL-10.2 mg/dL)||10.1|
|Glucose||110 (range: 70 mg/dL-140 mg/dL)||102|
Table 1: Laboratory results of the Patient.
On neurological examination, he was oriented to place, person and time, but required constant stimulation to remain awake and was notable for mild photophobia No nuchal rigidity, Kernig or Brudzinski’s signs were noted. His strength was intact and sensory examination was unremarkable. His gait examination was deferred given general weakness, and lethargy. The remainder of his neurological examination was unremarkable.
After a normal head CT without contrast and subsequent MRI of the brain with and without gadolinium, lumbar puncture findings including cerebrospinal fluid pleocytosis, elevated protein and positive WNV IgM antibody confirmed the diagnosis of WNV meningoencephalitis. The results of the cerebrospinal fluid (CSF) analysis and microbial work-up are detailed in Table 2 and Table 3 respectively.
|CSF analysis (Day1)|
|WBC||1243 (range 0 cubic mm-5 cubic mm)|
|Glucose||50 mg/dL (range 45 mg/dL-80 mg/dL)|
|RBC||0 (range: negative)|
|Total protein||196.2 mg/dL (range: 20 mg/dL-40 mg/dL)|
|Microscopy||No bacteria seen,polymorpho. Neutrophils, and mononuclear cells present|
Table 2: Cerebrospinal fluid analysis.
|Ehrlichiachaffeensis Antibody||CSF||IgG Antibody|
|Typhus fever group||CSF||Antibody Panel:|
|Enterovirus||CSF||No RNA detected by PCR|
|West-Nile virus antibody||CSF||Negative for WNV IgG|
|Positive for WNV AbIgM (Ref: Negative)|
|Bacterial culture||CSF||Negative after 72 h|
|Herpes simplex type I, or type II||CSF||Negative by PCR detection|
|Bacterial culture||Blood||No growth|
|Bacterial culture||Urine||<10,000 CFU/ml mixed gram positive organisms|
|Tuberculosis quantiferon B||Blood||Negative TB by QuantiFERON, B|
|TB Antigen value: 0.02IU/mL (Ref: <0.3IU/mL)|
|West Nile virus, Serum||Blood||Positive for IgG antibody|
|Positive for IgM antibody|
|Syphilis serology||Blood||Nonreactive (ref: non-reactive)|
Table 3: Microbiology work-up during admission.
|California/Lacrosse Encephalitis Profile||Blood||Negative|
|Western Equine Encephalitis||Blood||Negative|
|West Nile virus, Serum||Blood||Positive for IgG antibody|
|Positive for IgM antibody|
|Eastern Equine Encephalitis||Blood||Negative|
Table 4: Mosquito-Borne Panel.
Additional extensive infectious work-up including work up for mosquito borne viruses and other potential infectious etiologies was negative (Tables 3 and 4 respectively). Serum laboratory work-up included CBC, liver function tests, pancreatic function tests, lipid profile, electrolytes, and urinalysis. This revealed elevated levels of amylase and lipase. Ultrasound of the pancreas, liver, and gallbladder revealed mild dilation of the common bile duct without evidence of choledolithiasis, pancreatic ductal dilatation or peripancreatic fluid. No pancreatic calcifications or pseudocysts were noted. The liver appeared of normal echogenicity without intrahepatic lesions. Based upon our work-up, the patient was diagnosed with WNV meningoencephalitis with concurrent pancreatitis.
In the hospital, he received aggressive intravenous hydration with normal saline, made NPO, and treated with Ondansetron for nausea, oxycodone for abdominal pain, and pantoprazole for gastrointestinal prophylaxis.
This patient’s hospitalization course significant for persistent debilitating headaches, associated with nausea, vertigo and dizziness. His abdominal pain persisted for the first 6 days following his admission, with several failed attempts at advancing his diet from clear liquids to regular texture. After one week of hospitalization, the patient began to gradually improve, with decreased requirement for narcotics and anti-emetics. By day 9 post-admission, he was able to tolerate a regular diet. He was evaluated by physical therapy the following day, who noted that he had made a remarkable recovery and may be safe to be discharged home. He was eventually discharged home approximately 2 weeks following his admission. This patient’s symptoms fully resolved approximately 3 weeks from their onset.
The primary vector for the transmission of WNV is the Culex mosquitos’ genus, but other genera have also been implicated . In Europe, the principal vectors are C. pipiens, C. univittatus., and C. antennatus, and in India, C. vishnui [7,8]. In Northern America, more than 59 different mosquito species with diverse ecology and behavior have been implicated, but only approximately 10 of these are considered to be the principal WNV vectors (CDC, unpublished data) [6,8,9]. In 2001, 57% of these positive mosquito pools in the Northeastern US were C.pipiens or the Northern house mosquito, which feeds primarily on birds and mammals’ blood [4,6]. Although infected mosquito bites are the primary form of transmission, nonmosquito borne WNV transmission has also been documented in the literature . By 2002, four novel routes of WNV transmission to human had been identified: blood transfusion, organ-transplant recipient, trans-placental infection, and breast-feeding . The patient described in this case lived in Northern New England, an area not known to be endemic for WNV. This case illustrates the first clinical presentation of WNV meningo-encephalitis with concomitant pancreatitis in North America. In our patient, this was confirmed by history, physical examination, and serological markers.
Since IgM does not cross the blood-brain barrier, detection of CSF WNV IgM strongly suggests CNS involvement with WNV . IgG titers usually become detectable within 7-21 days in patient presenting with acute WNV infections . We excluded other mosquito-borne virus and other causes of pancreatitis, such as alcohol, gallstone, medication, hyperkalemia, and spider bites by history, physical examination, imaging and laboratory investigations.
It is important to note that acute pancreatitis was not detected by abdominal imaging. Trans abdominal ultrasonography has only a limited role when diagnosing acute pancreatitis due to operator dependence, difficulty with pancreatic necrosis detection, and restricted visualization secondary to abdominal pain or intraabdominal gas.
This case illustrates a very rare complication of WNV infection. The association of fever, headache, lethargy, persistent vertigo, dizziness and the CSF findings, along with abdominal pain, nausea, anorexia and elevated serum lipase/amylase levels in our patient’s suggest that the etiology of pancreatitis was induced by WNV. This emulates the neural-infection with enterovirus or mumps complicated by acute pancreatitis.
Due to the paucity of reports of patients with acute WNV pancreatitis, it is difficult to identify patients at risk of developing WNV pancreatitis during the acute phase of WNV neural infection. Our case illustrates that, in WNV encephalitis patients presenting with abdominal pain and vomiting, pancreatitis related to their infection, rather than just a separate entity, should be considered. Although treatment remains supportive at this point, the patient may benefit from a multidisciplinary approach.
- Platonov AE (2001) West Nile encephalitis in Russia: Were we ready? Are we ready? Ann N Y AcadSci 951:102-116.
- Campbell GL, Marfin AA, Lanciotti RS, Gubler DJ (2002) West Nile virus. Lancet Infect Dis 2: 519-529.
- Weinberger M, Pitlik SD, Gandacu D (2001) West Nile fever outbreak, Israel 2000: epidemiologic aspects. Emerg Infect Dis 7: 686-691.
- Hayes EB, Komar N, Nasci RS, Montgomery SP, O'Leary DR (2005) Epidemiology and transmission dynamics of West Nile virus disease. Emerg Infect Dis 11: 1167-1173.
- Sejvar JJ, Haddad MB, Tierney BC, Campbell GL, Marfin AA, et al. (2003) Neurological manifestations and outcome of West Nile virus infection. JAMA 290: 511-515.
- Komar N (2003) West Nile virus: Epidemiology and ecology in North America. Adv Virus Res 61: 185-234.
- Ceausu E, Erscoiu S, Calistru P, Dorobat B, Simion CV, et al. (1997) Clinical manifestations in the West Nile virus outbreak. Rom J Virol 48: 3-11.
- Nash D, Mostashari F, Fine A, Jammer K, Dominic S, et al. (2001) The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med 344: 1807-1814.
- Chowers MY, Lang R, Nassar F, Ericson D, Francis P, et al. (2001) Clinical characteristics of the West Nile fever outbreak, Israel, 2000. Emerg Infect Dis7: 675-678.
- Southam CM, Moore AE (1954) Induced virus infections in man by the Egypt isolates of West Nile virus. Am J Trop Med Hyg 3: 19-50.
- Guharoy R, Gilroy SA, Noviasky JA, Ference J (2004) West Nile virus infection. J Health Syst Pharm 61: 1235-1234.
- Lanciotti RS, Kerst AJ, Nasci RS, Anset P, Loci B, et al. (2000) Rapid detection of West Nile virus from human clinical specimens, field-collected mosquitoes, and avian samples by a Taq- Man reverse transcriptase-PCR assay. J ClinMicrobio38: 4066-4071.
- Petersen LR, Marfin AR (2002) West Nile virus: a primer for the clinician. Ann Intern Med 137: 173-179.
- Mostsahari F, Bunning ML, Kitsutani PT (2001) Epidemic West Nile encephalitis, New York, 1999: results of a household based seroepidemilogical study. Lancet 358: 261-264.
- Tsai TF, Popovici F, Cernescu C, Campbell GL(1998) West Nile encephalitis epidemic in southeastern Romania. Lancet 352: 767-771.
- Buber J, Fink N, Bin H, Mouallem M (2008) West Nile virus-induced pancreatitis. Travel Med Infect Dis 6: 373-375.
- Perelman A, Stern J (1974) Acute pancreatitis in West Nile Fever. Am J Trop Med Hyg 23: 1150-1152.
- Solomon T, Vaughn DW (2002) Pathogenesis and clinical features of Japanese encephalitis and West Nile virus infections. Curr Top MicrobiolImmunol267: 171- 194.
- Zeller HG, Schuffenecker I (2004) West Nile virus: an overview of its spread in Europe and the Mediterrerranean basin in contrast to its spread in the Americas. Eur J ClinMicrobiol Infect Dis 23: 147-156
- Hayes CG, Monath TP (2005) West Nile fever In: The arboviruses: epidemiology and ecology, vol. V. Boca Raton (FL): CRC Press; 1989. P. 59-88.West Nile virus epizootiology in the southeastern United States Vector Borne Zoonotic Dis 5: 82-89
- Turell MJ, Dohm DJ, Sardelis MR, Oguinn ML, Andreadid TG, et al. (2005) An update on the potential of north American mosquitoes to transmit West Nile Virus. J Med Entomol42: 57-62.
- Hayes EB, O’Leary DR (2004) West Nile virus infection: a pediatric perspective. Pediatrics 113: 1375-1381.
- Olejnik E (1952) Infectious adenitis transmitted by Culexmolestus. Bulletin of the Research Council of Israel 2: 210-211.
- Goldblum N, Sterk VM, Paderski B (1954) The clinical features of the disease and the isolation of West Nile virus from the blood of nine human cases. Am J Hygiene 59: 89–103
- Pealer LN, Marfin AA, Petersen LR ,Crimson R, Johnson K, et al. (2002) Transmission of West Nile virus through blood transfusion in the United States in 2002. N Engl J Med349: 1236-1245.
- De biasi RL (2003) Update: detection of West Nile virus in blood donationsUnited States.MMWR Morb Mortal Wkly Rep 52: 916-919.
- Centere for disease control and prevention (2002) Intrauterine West Nile virus infection New York. MMWR Morb Mortal Wkly Rep51: 1135-1136.
- Centere for disease control and prevention (2002) Possible West Nile virus transmission to an infant through breast-feeding-Michigan (2002) MMWR Morb Mortal Wkly Rep 51: 877-878.
- Update: detection of West Nile virus in blood donationsUnited States.MMWR Morb Mortal Wkly Rep 52: 916-919.
- Intrauterine West Nile virus infection New York. MMWR Morb Mortal Wkly Rep51: 1135-1136.
Citation: Babi MA, Waheed W, Wardi S (2016) A First Clinical Case Report of West-Nile Viral Meningoencephalitis Complicated with Acute Pancreatitis in North America. J Meningitis 1:104. Doi: 10.4172/2572-2050.1000104
Copyright: ©2016 M-Alain Babi, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Select your language of interest to view the total content in your interested language
Share This Article
March 08-09, 2018 London, UK
May 16-17, 2018 Osaka, Japan
July 12-13, 2018 Paris, France
December 05-06, 2018 Chicago, USA
- Total views: 8253
- [From(publication date): 6-2016 - Jan 18, 2018]
- Breakdown by view type
- HTML page views: 8154
- PDF downloads: 99