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There are seventeen species of birds that are the known carriers of and transmit West Nile Encephalitis (WNE) to humans via the Culex, Aedes, and Anopheles mosquitoes. WNE first causes symptomatic or asymptomatic illness in wild migratory birds that act as viral replication factories. Wild birds infected with WNE contain high titers of the virus and remain viremic for 1-2 weeks, making them ideal hosts to perpetuate the disease. Mosquitoes transmit WNE from birds to humans. Horses, dogs, and other small animals may harbor WNE after being bitten; however, they are inefficient transmitters because viral titers are relatively low, and WNE viremia is short-lived in these animals.
Patients with WNE may present with a wide range of severity in symptoms and may features of encephalitis, aseptic meningitis (meningoencephalitis), or both. It is common for patients to have a mild febrile illness accompanied by headache, mental confusion, tremors, or flaccid paralysis. Symptoms are most obvious in people who are very young and people who are elderly. Many people who are infected (at least most children) are also often asymptomatic or have a nonspecific flu-like illness. A minority of people may develop neurologic disease.
The extent and severity of viral invasion of the central nervous system (CNS) determine the clinical expression of WNE. Most patients are febrile or have low-grade fevers. Patients presenting with encephalitis have mental confusion or disorientation and may have decreased consciousness. Patients with severe cases of WNE may present with stupor or coma. The most common ophthalmic manifestation for WNE is chorioretinitis and about 10% of patients have an enlarged liver and spelnomegaly. CNS findings include a stiff neck with meningeal signs, including positive Kernig or Brudzinski signs in patients with aseptic meningitis or meningoencephalitis. Generalized adenopathy and an enlarged submental node are also very common.
Mosquito bites are the main culprits for the spread of WNE with an incubation period of WNE is 1-6 day but many patients may not provide a mosquito bite history. WNE usually occurs in the summer when mosquitoes, wild migratory birds, and humans are in close proximity outdoors. Mosquito bites, which are particularly prone to occur during feeding times (dawn and dusk) in the summer months, transmit WNE and prolonged contact or multiple mosquito bites enhances risk.
WNE may be transmitted in organ transplants and WNE virus has been found in breast milk.
WNE, as with other arthropod-borne viral encephalitis, traverses the blood-brain barrier and infects the brain parenchyma, clinically manifesting as viral encephalitis. WNE may also affect the leptomeninges, resulting in a clinical presentation of aseptic meningitis (viral meningitis). Patients with WNE may present with features of both encephalitis and aseptic meningitis (meningoencephalitis).
In the US the initial cases of WNE were first identified in the greater New York area, but cases have now occurred in western states. Wild birds with WNE virus have also been identified in parts of Canada. WNE is common in the Middle East, Asia, and Africa WNE seropositivity of children in Egypt is approximately 50%. WNE is the most common cause of viral aseptic meningitis or encephalitis in patients presenting to emergency departments in Cairo. Both sexes are affected equally and it is more frequent in elderly patients.
Encephalopathy is a feature of many systemic illnesses that presents with encephalitis. Most of these patients have extra-CNS findings that suggest the underlying disease process. Common disorders with CNS manifestations that may mimic WNE include subacute bacterial endocarditis, Legionnaires Disease, Rocky Mountain Spotted Fever, Epstein-Barr virus infectious mononucleosis, human herpesvirus 6, and systemic lupus erythematosus cerebritis.
Enteroviral aseptic meningitis
The most common cause of aseptic meningitis encountered during the summer months is enteroviral meningitis. Enteroviral aseptic meningitis is most commonly due to coxsackieviruses but may also be due to enterocytopathogenic human orphan virus or nonparalytic strains of poliovirus. Enteroviral meningitis may occur after water exposure in swimming pools, lakes, streams, or oceans as well as after contact with infected individuals.
Acute enteroviral CNS infections usually manifest as aseptic meningitis, uncommonly as meningoencephalitis, or rarely as encephalitis. Nonexudative pharyngitis, maculopapular extremity rash, loose stools, and even diarrhea often accompany enteroviral aseptic meningitis, which provides clues to its presence.
Enteroviral meningitis is not accompanied by paralysis or prolonged and/or profound lymphopenia.
Electroencephalogram: This is the most sensitive way to make a presumptive diagnosis of HSV-1 encephalitis. An abnormal temporal lobe focus is present on EEG as early as the first few days of the disease.
EEG shows unilateral focal electrical abnormalities in the temporal lobe.
Lumbar puncture: CSF reveals mild-to-moderate pleocytosis with a lymphocytic predominance in WNE. CSF protein is variably elevated, and the CSF glucose level is not decreased.
The CSF lactic acid level is not elevated, and RBCs, excluding traumatic taps, are not present in WNE. CSF Gram stain and bacterial culture findings are negative.
Provide supportive care to minimize the potential for cerebral edema. In comatose patients, pay special attention to maintaining a clear airway. Fluid replacement is also essential.
No surgical care is necessary.
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Report last updated: 2008/01/29 00:00:00 GMT+0