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Large thrombi from the leg veins may wedge themselves at the bifurcation of the pulmonary artery. West Nile virus (WNV) is a neurotropic virus that produces damage of varying severity and anatomic predilection.
WNV was first recognized in the Western hemisphere in August 1999 when a report of 62 patients with meningoencephalitis, sometimes associated with weakness, was published in New York. Since its introduction, the virus has spread West and South to involve the majority of the continental United States.
The virus is amplified in birds and is transmitted to humans most commonly through infected Culex mosquito bites. Fortunately, most of the WNV seroconversions are subclinical, with overt clinical illness affecting 1 in 100 to 1 in 150 patients. WNV is a member of the Japanese encephalitis complex of viruses that also includes the Japanese encephalitis virus and St. After a phase of initial replication and seeding of the reticuloendothelial system, a secondary viremia occurs with seeding of the central nervous system (CNS).
Viremia is usually a transient phenomenon that precedes onset of symptoms and disappears with development of specific immunoglobulin (Ig) G and IgM antibodies. Risk factors for increased mortality include host characteristics such as older age (>75 years), diabetes mellitus, and level of immunosuppression, as well as measures of disease severity such as decreased level of consciousness, neuroimaging abnormalities, and the development of limb weakness. WNV shares with the other Japanese encephalitis complex viruses a tendency to cause encephalitis and, less often, aseptic meningitis and paralytic poliomyelitis. Those Flaviviruses, including WNV, infect neurons throughout the CNS, but more severely in certain sites appropriate for the different clinical syndromes. Prominent inflammation of the brainstem was pathologically confirmed in patients with bulbar and ophthalmoplegic symptoms. Acute flaccid paralysis observed in WNV was correlated in multiple studies with perivascular lymphocytic infiltration and neuronophagia of the anterior horn cell region, similar to poliomyelitis.
Although the presence of specific viral receptors on motor neurons explains the anterior horn cell neurotropism with polioviruses, the pathogenesis of the preferential rostral and anterior horn cell infection with WNV remains poorly understood.
Reduced level of consciousness, a general symptom of encephalitis, is often associated with other, more localizing signs such as tremor, bulbar dysfunction, ataxia, or focal weakness, reflecting more specific areas of CNS involvement.
Focal weakness develops in around one half of patients with WNV CNS infection, with progression to frank paralysis in up to 35%. Earlier studies suggested that older age and medical comorbid conditions could predispose to weakness. In contrast to the headache and mental status alterations that are the usual manifesting symptoms, weakness often evolves and develops in the subacute phase of the illness. The limb weakness is of a lower–motor neuron pattern, with flaccid tone, areflexia, or hyporeflexia.
The clinical pattern consists of flaccid quadriparesis, asymmetrical paraparesis, or monoparesis. The weakness typically involves proximal musculature, and the upper lumbar segments can be affected in isolation, mimicking an upper lumbar radiculopathy or plexopathy. Other neurologic manifestations include movement disorders, rhombencephalitis, and cerebellar dysfunction. Rhombencephalitis with associated bulbar dysfunction and swallowing difficulties can contribute to morbidity and prolonged hospitalization. Most of the salient neurologic manifestations become obvious several days or even weeks into the illness, as the patient is recovering from the meningoencephalitis and beginning rehabilitation. Complete blood counts on admission usually show no major abnormalities, although there may be absolute or relative lymphopenia. Up to one third of the patients develop significant hyponatremia, compatible with the syndrome of inappropriate antidiuretic hormone secretion, either during their illness or in the recovery period.
These CSF findings support a diagnosis of meningitis or meningoencephalitis and help to exclude other conditions, such as Guillain-Barré syndrome, which is the main differential diagnostic consideration in patients with a rapidly progressive flaccid paralysis. Reactive or atypical lymphocytes and Mollaret's cells, the monocyte variants originally described with recurrent aseptic meningitis, have also been reported and can be helpful in making the appropriate diagnosis. In more than 70% of the cases with acute flaccid paralysis, nerve conduction studies show reduced or absent compound motor action potentials with preserved sensory nerve action potentials, conduction velocities, and distal latencies.
Such a pattern suggests anterior horn cell disease with or without additional motor root involvement, as is seen with poliomyelitis.
This pattern was previously attributed to a possible peripheral sensorimotor polyneuropathy but is now believed to represent dorsal root ganglia inflammation in the context of a myelitis.
Only a handful of cases have been reported to show electrodiagnostic findings compatible with an isolated demyelinating process or a combination of axonal and demyelinating processes. Needle electrode examinations show abnormal spontaneous activity such as fibrillation potentials and positive sharp waves in the acute setting, reflecting active denervation.


Needle electrode examinations and nerve conduction studies can be abnormal in clinically unaffected muscles, reflecting a more widespread involvement with the WNV. Needle electrode examinations and nerve conduction studies at 8 months after disease onset show chronic denervation and motor axon loss in affected limbs.
No acute abnormalities are detected in computed tomographic scans of the brains of patients with acute WNV infection. Similar changes were described in the thalamus, cerebellum, and brainstem in patients with prominent cerebellar, parkinsonian, or brainstem symptoms. In patients with WNV-associated flaccid paralysis, MRI of the spine is abnormal in 75% with T2 and FLAIR hyperintensities involving the cord parenchyma at the level of the cervical or lumbar cord, and gadolinium enhancement in the cauda equina compatible with myeloradiculitis.
The treatment of WNV is currently supportive, with particular attention to the risk of respiratory compromise secondary to muscle weakness and aspiration secondary to bulbar dysfunction. Lifestyle modifications include avoiding outdoor activities during the hours around dawn and dusk, when mosquitoes are most active, and wearing protective, light-colored clothing to limit insect bites.
A vaccine has been developed for veterinary use in horses but is not approved for use in humans.
One study evaluating patients at 18 months following acute infection suggested a somewhat higher mortality rate (around 30%), mostly in patients initially presenting with respiratory failure.
Patients with WNV myelitis show no improvement in limb weakness if flaccid paralysis develops. The persistence of movement disorders is a less-defined feature, with conflicting results in various studies. Although central nervous system involvement with West Nile virus (WNV) infection is rare, it can be devastating. Neurologic manifestations are very variable, mainly including meningitis, encephalitis, and a polio-like limb weakness.
Long-term outcome studies suggest persistent weakness and neurocognitive complaints in up to one half the patients affected.
Possible benefit of intravenous immunoglobulin therapy in a lung transplant recipient with West Nile virus encephalitis.
The prevalence of arboviral, rickettsial, and Hantaan-like viral antibody among schoolchildren in the Nile river delta of Egypt.
Possible West Nile virus transmission to an infant through breastfeeding—Michigan 2002.
Estimated risk of West Nile virus transmission through blood transfusion during an epidemic in Queens, New York City. West Nile virus infection in 2002: Morbidity and mortality among patients admitted to hospital in southcentral Ontario.
B cells and antibody play critical roles in the immediate defense of disseminated infection by West Nile encephalitis virus.
Mouse neuroinvasive phenotype of West Nile virus strains varies depending upon virus genotype. Neurological features of West Nile infection during the 2000 outbreak in a regional hospital in Israel. During an ongoing infection, however, your immune system is unable to conquer the bacteria on its own and the pain and redness continue to worsen. When your infection has a burst of activity, or when there are signs that this is about to occur, your general dentist may recommend you see a periodontist. If you notice any of the above warning signs of periodontal infection, please contact your general dentist and ask for a periodontal evaluation. A periodontist is a dentist who specializes in the prevention, diagnosis and treatment of periodontal disease.
That’s the meaning of the name rambutan fruit – and an great description of the fruit as well.
According to popular belief and the origin of its name, rambutan is native to Indonesia and Malaysia. The earliest record of rambutan trees show that they were cultivated by the Malayan jungle tribes around their temporary settlements, a practice followed to date. Rambutan trees grow naturally throughout Southeast Asia, although their precise natural distribution is unknown. It is closely related to several other edible tropical fruits including thelychee, longan, and mamoncillo. It is native to the Indonesian Archipelago, from whence it spread westwards to Thailand, Burma, Sri Lanka and India, and northwards to Vietnam and the Philippines. The flesh exposed when the outer skin is peeled off is sweet and sour, slightly grape-like and gummy to the taste. This fruit is a traditional medicine in Malaysia and Indonesia that is being used for hundreds of years.
It is used in a number of treatments which includes diabetes, hypertension and various other ailments.
The carbohydrates and protein content of rambutan help to increase energy and prevent bloating.


Rambutan is also rich in water which helps to get back the lost energy and quenches thirst. This compound behaves like a free radical scavenger that protects our body from oxidative damage and is particularly helpful to fight cancer. This fruit contains moderate amounts of copper which is necessary for the creation of white and red blood cells. Phosphorus in rambutan helps to remove the waste in kidneys and is essential for the development, repair, and maintenance of tissues and body cells. Rambutan also contains significant amounts of Calcium which works together with phosphorus to fortify the teeth and strengthens bones.
Rambutans are an excellent source of iron which helps to correct the amount of oxygen in the body which controls dizziness and fatigue due to anaemia, an illness caused by iron deficiency. The fruit keeps us full for a long time due to its high fiber and water content and controls irregular hunger pangs. Consuming the fruit can help to kill intestinal parasites and helps to relieve symptoms of diarrhoea and fever.
Due to its ability to scavenge free radicals, Rambutan protects your body from oxidative damages.
Bech's Organic Pili Nut Farm copyright 2015 - All rights ReservedChris Bech Sustainable Investments - BEACH LAND ESTATE Inc. Mix and match pamphlet design packages, buy more than 50 packages (2,500 pamphlets) and get 1 dollar off each pack. When the reactive inflammatory processes are restricted to the meninges, an aseptic meningitis with headache as the chief manifestation results. An exponential increase in WNV activity in the United States was observed, with at least 3737 cases and 201 fatalities in 2002. Transmission through blood transfusion, organ transplantation, and breast-feeding have also been reported. This appears to be due to the strength of the host immune system but could partly be due to the difference in severity of neurovirulence among different WNV strains. More severe infections of the basal ganglia and thalamus, as suggested by neuroimaging were found in patients with prominent parkinsonism and movement disorders. More characteristic features include back or limb pain in around one third of the patients. Physical examination usually reveals hyperreflexia, as would be expected with upper motor neuron injury, unless there is associated myelitis, where areflexia becomes the rule. It is typically asymmetrical and rapidly progressive, reaching nadir weakness within 2 to 8 days of symptom onset.
Although weakness usually occurs in the context of encephalitis, cases of isolated limb involvement have also occurred without the other features of headache or encephalopathy, posing a diagnostic challenge. Movement disorders such as parkinsonism, with rigidity, bradykinesia, and gait changes, were described in up to 69% of hospitalized WNV patients in one series.
Although the tremors can be mistaken for seizure activity in severely affected patients, focal motor seizures have rarely also been described.
However, immunosuppressed patients exhibit a prolonged period of viremia and a delayed antibody response. Approaches to prevention include reduction of the mosquito population with draining of water from mosquito breeding sites and use of mosquito larvicides and maturation inhibitors to reduce the numbers of mosquitoes. The virus can cause salient neurologic manifestations ranging from aseptic meningitis to flaccid quadriplegia.
This infection leads to an inflammation under the gums, and if not treated, this inflammation can destroy the bone around your teeth. As ongoing research continues to define how periodontal disease is associated with these and other health problems, oral health maintenance is essential. To be certain about any periodontal disease, ask your dentist or periodontist to examine your gums for signs of infection. With additional brain parenchymal involvement, altered level of consciousness accompanies the headache and reflects the associated meningoencephalitis. This virus group belongs to the Flaviviridae, a family of single-stranded RNA viruses transmitted by arthropods, mostly Culex mosquitoes in the case of WNV. One fourth of patients have a nonpurulent, maculopapular erythematous rash, usually antedating any neurologic manifestations by several days. Heightened awareness is essential for early diagnosis, and prevention remains crucial in the absence of effective targeted therapy.
Periodontists receive extensive training in these areas, including 2 to 3 additional years of education beyond dental school. Lancinating pains and focal areflexic weakness denote a myelitis, with inflammation of the spinal cord.



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