Susceptibility and Pathogenesis of Eurasian Tree Sparrows Experimentally Inoculated with Velogenic Newcastle Disease Virus.

Wild-caught Eurasian tree sparrows (Passer montanus) were experimentally inoculated with genotype VII velogenic Newcastle disease virus (NDV) APMV1/chicken/Japan/Fukuoka-1/2004 to investigate the susceptibility and pathogenesis of infected sparrows. Intranasal inoculation of two groups with high or low doses of the virus resulted in the mortality of some birds in both groups on days 7-15 postinoculation. Neurologic signs, ruffled feathers, labored breathing, emaciation, diarrhea, depression, and ataxia were observed in a few birds that eventually succumbed to death. The inoculation of the higher viral load resulted in higher mortality and hemagglutination inhibition antibody detection rates. Tree sparrows that survived the 18-day observation period after inoculation exhibited no apparent clinical signs. Histologic lesions in dead birds were observed in the nasal mucosa, orbital ganglion, and central nervous system, accompanied by NDV antigens detected by immunohistochemistry. Viral inclusion bodies were rarely observed in the cytoplasm of neurons. NDV was isolated from the oral swab and brain of dead birds but not from other organs, including the lung, heart, muscle, colon, and liver. In another experimental group, tree sparrows were intranasally inoculated with the virus and then examined 1-3 days later to examine the early pathogenesis of the disease. Inoculated birds exhibited inflammation of the nasal mucosa with viral antigens, and virus was isolated from some oral swab samples on days 2 and 3 postinoculation. The results of the present study suggest that tree sparrows are susceptible to velogenic NDV, and the infection could be fatal, although some birds can exhibit asymptomatic or mild infection. The unique pathogenesis regarding the neurologic signs and viral neurotropism of velogenic NDV was characteristic in infected tree sparrows.

Susceptibilidad y patogenia en los gorriones molineros inoculados experimentalmente con un virus velogénico de la enfermedad de Newcastle. Gorriones molineros (Passer montanus) capturados de la naturaleza se inocularon experimentalmente con un virus velogénico de la enfermedad de Newcastle (NDV) del genotipo VII APMV1/chicken/Japan/Fukuoka-1/2004 para investigar la susceptibilidad y la patogenia de los gorriones infectados. La inoculación intranasal de dos grupos con dosis altas o bajas del virus resultó en la mortalidad de algunas aves en ambos grupos en los días siete a 15 posteriores a la inoculación. Se observaron signos neurológicos, plumas erizadas, dificultad para respirar, emaciación, diarrea, depresión y ataxia en algunas aves que finalmente sucumbieron a la muerte. La inoculación de la carga viral más alta resultó en tasas más altas de detección de anticuerpos inhibidores de hemaglutinación y mortalidad. Los gorriones molineros que sobrevivieron al período de observación de 18 días después de la inoculación no mostraron signos clínicos aparentes. En las aves muerta se observaron lesiones histológicas en la mucosa nasal, ganglio orbitario y sistema nervioso central, acompañadas de antígenos virales detectados por inmunohistoquímica. Rara vez se observaron cuerpos de inclusión virales en el citoplasma de las neuronas. El virus de Newcastle se aisló del hisopo orales y del cerebro de aves muertas, pero no de otros órganos, incluidos los pulmones, el corazón, los músculos, el colon y el hígado. En otro grupo experimental, el virus se inoculó por vía intranasal a los gorriones molineros y luego se examinaron al día uno y tres para examinar la patogenia temprana de la enfermedad. Las aves inoculadas exhibieron inflamación de la mucosa nasal con antígenos virales y se aisló el virus de algunas muestras de hisopos orales en los días dos y tres posteriores a la inoculación. Los resultados del presente estudio sugieren que los gorriones molineros son susceptibles al virus de Newcastle velogénico y que la infección podría ser mortal, aunque algunas aves pueden presentar una infección asintomática o leve. La patogénesis única con respecto a los signos neurológicos y el neurotropismo viral del virus de Newcastle velogénico fue característica en los gorriones molineros infectados.

Perindopril increases the swallowing reflex by inhibiting substance P degradation and tyrosine hydroxylase activation in a rat model of dysphagia.

Patients with hypertension have a high risk of ischemic stroke and subsequent stroke-associated pneumonia. Stroke-associated pneumonia is most likely to develop in patients with dysphagia. The present study was designed to compare the ameliorative effects of different treatments in rat model of dysphagia. Spontaneously hypertensive rats were treated with bilateral common carotid artery occlusion (BCAO) to induce chronic cerebral hypoperfusion causing disorders of the swallowing reflex. Angiotensin-converting enzyme (ACE) inhibitors (perindopril, imidapril and enalapril), an angiotensin II type 1-receptor blocker (losartan), a vasodilator (hydralazine) and an indirect dopamine agonist (amantadine) were dissolved in drinking water and administered to the rats for six weeks. The blood pressure, the swallowing reflex under anesthesia, the substance P content in the striatum and the tyrosine hydroxylase (TH) expression in the substantial nigra were measured. Compared to the vehicle control, the decrease in the swallowing reflex induced by BCAO was attenuated significantly by enalapril, imidapril and perindopril, but only slightly by losartan. Hydralazine had no effect on the swallowing reflex. Amantadine significantly attenuated the decreased swallowing reflex but increased the blood pressure. Cerebral hypoperfusion for six weeks decreased the TH expression and substance P level. Perindopril improved both the TH expressions and substance P level, but imidapril, enalapril and amantadine only improved the substance P level. The present findings indicate that perindopril could be useful for preventing dysphagia in the chronic stage of stroke by attenuating the decrease in TH expression and the decrease in the substance P level.

Bozasella gracilis n. sp. (Ciliophora, Entodiniomorphida) from Asian elephant and phylogenetic analysis of entodiniomorphids and vestibuliferids.

Bozasella gracilis n. sp. in the order Entodiniomorphida was found in fecal samples of an Asian elephant kept in a zoo. The ciliate has general and infraciliary similarities to the families Ophryoscolecidae and Cycloposthiidae. Phylogenetic trees were inferred from 18S rRNA gene sequences of B. gracilis, 45 entodiniomorphids, 10 vestibuliferids, 5 macropodiniids, and an outgroup, using maximum likelihood, Bayesian inference, and neighbor joining analyses. Of them, there were 32 new sequences; 26 entodiniomorphid species in the genera, Bozasella, Triplumaria, Gassovskiella, Ditoxum, Spirodinium, Triadinium, Tetratoxum, Pseudoentodinium, Ochoterenaia, Circodinium, Blepharocorys, Sulcoarcus, Didesmis, Alloiozona, Blepharoconus, Hemiprorodon, and Prorodonopsis, and 6 vestibuliferid species in the genera, Buxtonella, Balantidium, Helicozoster, Latteuria, and Paraisotricha. Thirty additional sequences were retrieved from the GenBank database. Phylogenetic trees revealed non-monophylies of the orders Entodiniomorphida and Vestibuliferida, the suborders Entodiniomorphina and Blepharocorythina, and the families Cycloposthiidae and Paraisotrichidae. Bozasella gracilis was sister to Triplumaria. In addition, to avoid homonymy, we propose Gilchristinidae nom. nov., Gilchristina nom. nov. and Gilchristina artemis (Ito, Van Hoven, Miyazaki & Imai, 2006) comb. nov.