Sandbox ammu WNV EPi: Difference between revisions
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Latest revision as of 18:41, 18 September 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.
Overview
Universal screening for WNV is not recommended. As blood and transplant-related transmissions of the virus have been reported, nucleic acid tests (NAT) may be used to screen for WNV among potential blood and solid organ donors. In blood donation, individual screening is not recommended either. Instead, a "minipool" nucleic acid testing program (MP NAT) is implemented. Positive pools warrant further investigation for individuals. Patients with positive NAT may not donate blood or solid organs for at least 120 days. Re-testing after 120 days is indicated.
Screening
Universal screening for WNV is not recommended. Screening is only recommended for blood and solid organ transplant donors.
Screening donor blood products
Following the discovery of WNV transmission by blood transfusions, WNV blood donor screening is performed using nucleic acid testing (NAT). A "minipool" nucleic acid testing program (MP NAT) is currently implemented to detect WNV viremia among donors. In contrast, serological testing is not feasible for screening purposes because IgM seroconversion may be detectable approximately 5 months following infection.[1] Pools with positive NAT results warrant further investigation for individual screening. Individual patients with positive NAT may not donate blood for at least 120 days.[2][3][4][1]
Screening solid organ transplant donors
Although the only data on human-to-human transmission by organ transplantation is derived from reports that included deceased donors, transmission to recipients may still occur if donors have NAT-negative IgM-positive results. These findings suggest that clearance of the WNV from solid organs may be delayed compared to its clearance from plasma. Accordingly, screening for WNV among transplant donors is recommended using NAT. There is no evidence to demonstrate the optimal time for solid organ donation in cases of positive NAT, but re-testing after 120 days to confirm negative NAT has become common practice. Patients with negative results after 120 days may donate solid organs.[1]
References
- ↑ 1.0 1.1 1.2 "Identifying risk factors for West Nile virus (WNV) during evaluation of potential living donors" (PDF). United Network for Organ Sharing. The Organ Procurement and Transplantation Network. 2013. Retrieved 09/11/2014. Check date values in:
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(help) - ↑ Stramer SL, Fang CT, Foster GA, Wagner AG, Brodsky JP, Dodd RY (2005). "West Nile virus among blood donors in the United States, 2003 and 2004". N Engl J Med. 353 (5): 451–9. doi:10.1056/NEJMoa044333. PMID 16079368.
- ↑ Busch MP, Caglioti S, Robertson EF, McAuley JD, Tobler LH, Kamel H; et al. (2005). "Screening the blood supply for West Nile virus RNA by nucleic acid amplification testing". N Engl J Med. 353 (5): 460–7. doi:10.1056/NEJMoa044029. PMID 16079369.
- ↑ Kleinman S, Glynn SA, Busch M, Todd D, Powell L, Pietrelli L; et al. (2005). "The 2003 West Nile virus United States epidemic: the America's Blood Centers experience". Transfusion. 45 (4): 469–79. doi:10.1111/j.0041-1132.2005.04315.x. PMID 15819665.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [3]
Overview
West Nile fever must be differentiated from other diseases that cause fever, skin rash, myalgias, and back pain, such as other viral infections due to rhinovirus, enterovirus D68, coxsackievirus, influenza, echovirus. Patients with severe WNV infection may present with meningitis, encephalitis, or flaccid paralysis. These diseases must be differentiated from other diseases that cause severe headache, altered mental status, seizures, and paralysis, such as herpes virus encephalitis, enterovirus encephalitis, bacterial encephalitis, metabolic encephalitis, poliomyelitis, and Guillain-Barre syndrome.
Differential Diagnosis
Differential diagnosis of West Nile fever
Differential Diagnosis |
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Differential diagnosis of severe West Nile virus infection
West Nile Virus Presentation | Differential Diagnosis[1][2] |
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West Nile Virus Encephalitis and Meningitis | Herpes simplex virus, coxsackievirus, echovirus, other arbovirus, metabolic encephalopathy, bacterial meningitis, St. Louis encephalitis, eastern equine encephalitis virus, western equine encephalitis, Lyme disease. |
West Nile Virus Flaccid Paralysis | Acute poliomyelitis, Guillain-Barre syndrome, stroke, myasthenia gravis |
References
- ↑ Rossi, Shannan L.; Ross, Ted M.; Evans, Jared D. (2010). "West Nile Virus". Clinics in Laboratory Medicine. 30 (1): 47–65. doi:10.1016/j.cll.2009.10.006. ISSN 0272-2712.
- ↑ T. F. Tsai (1991). "Arboviral infections in the United States". Infectious disease clinics of North America. 5 (1): 73–102. PMID 1646839. Unknown parameter
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]
Overview
On physical examination, patients with WNV infection may have no specific signs. Physical examination findings may range from an isolated fever to signs of severe neurological impairment, meningeal irritation, stupor, and coma.
Physical exam
Most patients with WNV are asymptomatic or experience a mild disease that may often have no signs on physical examination.[1]
Vital signs
Skin
HEENT
- Papilledema
- Nystagmus
- Lymphadenopathy
- Non exudative pharyngeal erythema
Chest
- Ataxic or apneustic breathing
Abdomen
Neurologic
- Altered mental status
- Tremor
- Myoclonus
- Bradykinesia
- Rigidity
- Absent corneal reflex
- Absent gag reflex
- Memory loss
- Sensory loss
- Motor weakness
- Neck stiffness
- Positive Kernig and Brudzinski tests
- Hyperreflexia
- Positive Babinski reflex
References
- ↑ Sejvar JJ, Haddad MB, Tierney BC, Campbell GL, Marfin AA, Van Gerpen JA; et al. (2003). "Neurologic manifestations and outcome of West Nile virus infection". JAMA. 290 (4): 511–5. doi:10.1001/jama.290.4.511. PMID 12876094. Review in: ACP J Club. 2004 May-Jun;140(3):78
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [5]; Associate Editor(s)-in-Chief: Ammu Susheela, M.D. [6]
Overview
WNV is usually transmitted to humans by the culex mosquito after feeding on infected birds with high-level viremia. Following an incubation period of 2-14 day, untreated patients can remain asymptomatic or present with West Nile fever or with life-threatening neuroinvasive disease. Common complications of WNV infections include neurological impairment. The prognosis of mild disease is excellent; whereas West Nile meningitis and encephalitis may have residual neurologic deficits.
Natural History
WNV is a member of Japanese encephalitis antigenic complex of the family Flaviviridae. It is transmitted by a mosquito bite, most commonly Culex pipiens. Birds are the natural reservoir of the virus and the disease is generally transmitted to humans when a mosquito that previously fed on a bird with high-level viremia bites a human.[1]
Incubation Period
The incubation period for WNV disease is typically 2 to 6 days. It ranges from 2 to 14 days and can be several weeks in immunocompromised patients. An estimated 70-80% of human WNV infections are subclinical or asymptomatic. Less than 1% of infected individuals develop neuroinvasive disease, which typically manifests as meningitis, encephalitis, or acute flaccid paralysis.[2]
Asymptomatic West Nile Infection
When left untreated, approximately 80% of the people infected by virus remain asymptomatic.
West Nile Fever
Around 20% of the patients infected with WNV develop West Nile fever and usually present with fever and other constitutional symptoms. If left untreated, the infection generally self-resolves with no complications or sequelae.
Neuroinvasive Disease
Approximately 1 in 150 persons infected with WNV will develop a severe form of disease if left untreated. Serious illness can occur in patients of any age. However, advanced age, systemic diseases such as malignancy and cardiovascular disease, and immunosuppressed patients are considered high risk for developing neuroinvasive disease.
Possible complications
- Complications from mild West Nile virus infection are very rare.
- Complications from severe West Nile virus infection are as follows
Neurologic complications
- Meningitis
- Encephalitis
- Parkinsonism
- Rhomboencephalitis
- Cerebellar dysfunction
- West nile poliomyelitis [3]
- Dysphagia
- Permanent motor weakness
- Cranial nerve palsy
HEENT complications
Respiratory complications
Vascular complications
Other visceral organ complications
Prognosis
- In general, the prognosis of a mild WNV infection is excellent. Most patients with non-neuroinvasive WNV disease or WNV meningitis recover completely. However, fatigue, malaise, and weakness can linger for weeks or months.
- Patients who recover from WNV encephalitis often have residual neurologic deficits. Among patients with neuroinvasive disease, the overall case-fatality ratio is approximately 10%. The rate is significantly higher among patients with WNV encephalitis compared to patients with WNV meningitis.
References
- ↑ "West Nile Virus".
- ↑ "West Nile Virus".
- ↑ "Neurologic Complications of West Nile Virus".
- ↑ Perelman A, Stern J. "Acute pancreatitis in West Nile Fever." American Journal of Tropical Medicine and Hygiene 1974; 23: 1150-1152.
- ↑ Omalu B I, Shakir A A, Wang G, Lipkin W I, Wiley C A. "Fatal fulminant pan-meningo-polioencephalitis due to West Nile virus." Brain Pathology 2003; 13: 465-472
- ↑ Mathiot C C, Georges A J, Deubel V. "Comparative analysis of West Nile virus strains isolated from human and animal hosts using monoclonal antibodies and cDNA restriction digest profiles." Res Virol 1990; 141: 533-543.