, 2006). WNV-induced respiratory distress mechanisms have been extensively

studied in rodents and are discussed below. Cases of cardiac or renal involvement, although much less frequent, this website have been reported (Table 1). A case study of myocarditis has been reported in a patient having a confirmed case of WNV (Omalu et al., 2003). The patient developed cardiac arrhythmias and global myocardial dysfunction. Cardiac complications including arrhythmia are also described in a report of hospitalized patients with WNV disease (Bode et al., 2006). There are many reports of WNV-induced cardiac involvement in other mammalian (Lichtensteiger et al., 2003) and avian species (Gibbs et al., 2005). Electrocardiograms obtained from radiotelemetry in WNV-infected hamsters revealed some cardiac disturbances, but the implications on WNND have yet to be determined (Wang et al., 2011). In regards to renal function, 22% of patients with WNV-induced paralysis developed bladder dysfunction (Saad et al., 2005). A case study report claimed to be the first report of urological sequelae in a patient with WNV; the patient also had respiratory distress requiring intubation (Shpall et al., 2003). Other more subtle autonomic-like dysfunctions may also

occur in WNV neurological disease. For example, adrenal insufficiency, as detected by a corticotropin test, was identified in 70% patients with severe WNV www.selleckchem.com/products/otx015.html disease (Abroug et al., 2006). A central question is if autonomic dysfunction is due to direct Bacterial neuraminidase damage of motor functions or to damage of neurons generally regulating sympathetic or parasympathetic functions. Rodent studies using heart rate variability as an indicator of autonomic function, electromyography of the intestine and diaphragm, nerve conduction velocity, electrocardiography, plethysmography, and immunofluorescence assays indicated that WNV does cause some autonomic dysfunction, but many of these dysfunctions are caused by direct damage to motor functions (Morrey et al., 2012, Wang et al., 2011, Wang et al., 2013a and Wang et al., 2013b). Parkinsonism has been observed in 69% of WNV patients in one study (Sejvar et al., 2003a) (Table 1). Parkinson’s disease is a neurodegenerative

disease caused by death of dopaminergic neurons in the substantia nigra. Two WNV patients have been described by neuroimaging procedures with heavy involvement of the substantia nigra, which correlated with Parkinsonism features of the patient (Bosanko et al., 2003). It is not known if rodents have Parkinsonism, but hamsters infected with WNV manifest front limb tremors (Morrey et al., 2004b). No studies have been done to correlate these tremors with histopathogensis of infection of the substantia nigra. The other alternative mechanism of tremors that could be addressed with rodent models is hyper-excitability of neurons or synapses. In the mouse model of amyotrophic lateral sclerosis, limb tremors were associated with an elevation of excitatory synapses (Sunico et al., 2011).