Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors investigated an outbreak of West Nile Fever characterized by severe neurological symptoms and death in a flock of 3600 6-week-old geese. Ataxia, intermittent torticollis and opisthotonus, incoordination, rhythmic side-to-side movement of the head, wriggling of the neck and abnormal head position were features of the disease. Death occurred within 4 to 5 days after the clinical signs appeared. The average daily mortality was 5 to 15, reaching 14% (in total) over a period of 6 weeks. There were no consistent gross pathological lesions, but in a few cases yellowish-grey foci of 3 to 6 mm in diameter were observed on the surface or transection of the brain. Histopathology revealed perivascular lymphohistiocytic infiltration and glia cell proliferation in the brainstem, cerebellum, cortex and spinal cord as well as degeneration of neural fibres in the spinal cord. In addition to the lesions caused by the West Nile Virus in the brain, characteristics of circovirus infection such as lymphocyte depletion, vacuolization and basophilic intra-cytoplasmic inclusion bodies containing circovirus-like particles were seen by light and electron microscopy in the cloacal bursa. West Nile Virus infection was confirmed by reverse transcriptase-polymerase chain reaction amplification of virus-specific nucleic acid from tissue samples of the brain. Based on the nucleotide sequence analysis of the polymerase chain reaction products, 99% identity was found on the tested NS5 region with the IS-98 ST1 strain isolated from a stork in Israel in 1998, and with West Nile Virus stains emerging in the USA in 1999. Using an indirect fluorescent antibody test, high antibody titres against the virus were detected in the serum samples submitted from the affected flock. In selected sera this was confirmed by neutralization antibody test as well.
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PMID:Co-occurrence of West Nile Fever and circovirus infection in a goose flock in Hungary. 1623 74

Sixty-one birds of prey admitted to The Wildlife Center of Virginia (WCV; Waynesboro, Virginia, USA) from June to November 2003 were tested for West Nile virus (WNV) infection. Choanal and/or cloacal swabs were obtained and submitted to Virginia's Division of Consolidated Laboratory Services (Richmond, Virginia, USA) for analysis with real-time reverse transcriptase polymerase chain reaction (RT-PCR). Forty birds of prey were positive for WNV by RT-PCR. Five avian families and nine species of raptors were represented, with great horned owls (Bubo virginianus) and red-tailed hawks (Buteo jamaicensis) most frequently affected. Presenting clinical signs were consistent with previous reports of WNV infection in raptors; however, these differed between species. Of WNV positive birds, nonspecific signs of illness were the most common clinical findings, particularly in red-tailed hawks; signs included dehydration (n = 20), emaciation (n = 18), and depression (n = 15). Neurologic abnormalities were frequently identified, especially in great horned owls, and included head tremors (n = 17), ataxia (n = 13), head incoordination (n = 7), torticollis (n = 3), nystagmus (n = 3), and head tilt (n = 3). Great horned owls exhibited anemia and leukocytosis with heterophilia, eosinophilia, and monocytosis consistent with chronic inflammation. Red-tailed hawks were anemic with a heterophilic leukocytosis and regenerative left shift. The majority of WNV cases occurred during August and September; there was a marked increase in the number of raptors admitted to WCV during these months followed by a marked decrease during October, November, and December. This pattern differed from mean monthly admissions during the previous 10 years and suggests a negative impact on local raptor populations. The effects of WNV on avian populations are largely unknown; however, because of their ecological importance, further investigation of the effects of WNV on raptor populations is warranted.
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PMID:West Nile virus in raptors from Virginia during 2003: clinical, diagnostic, and epidemiologic findings. 1687 Aug 56

Asian H5N1 (hereafter referred to as panzootic H5N1) highly pathogenic avian influenza (HPAI) virus has caused large numbers of deaths in both poultry and wild-bird populations. Recent isolates of this virus have been reported to cause disease and death in commercial ducks, which has not been seen with other HPAI viruses. However, little is known about either the dissemination of this H5N1 within the organs or the cause of death in infected ducks. Nineteen 4-week-old Pekin ducks were infected with 10(6.7) median egg infectious doses of HPAI A/turkey/Turkey/1/05 (H5N1, clade 2.2) in 0.1ml via the intranasal and intraocular routes. Cloacal and oropharyngeal swabs were taken daily before three animals were selected randomly and killed humanely for postmortem examination, when samples of tissues were taken for real-time reverse transcriptase-polymerase chain reaction, histopathological examination and immunohistochemistry. Clinical signs were first observed 4 days post infection (d.p.i.) and included depression, reluctance to feed, in-coordination and torticollis resulting in the death of all the birds remaining on 5d.p.i. Higher levels of virus shedding were detected from oropharyngeal swabs than from cloacal swabs. Real-time reverse transcriptase-polymerase chain reaction and immunohistochemistry identified peak levels of virus at 2d.p.i. in several organs. In the spleen, lung, kidney, caecal tonsils, breast muscle and thigh muscle the levels were greatly reduced at 3d.p.i. However, the highest viral loads were detected in the heart and brain from 3d.p.i. and coincided with the appearance of clinical signs and death. Our experimental results demonstrate the systemic spread of this HPAI H5N1 virus in Pekin ducks, and the localization of virus in the brain and heart tissue preceding death.
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PMID:Pathogenesis of highly pathogenic avian influenza A/turkey/Turkey/1/2005 H5N1 in Pekin ducks (Anas platyrhynchos) infected experimentally. 1902 59

Six calves, aged between 55 days and 15 months, were presented between September and November 2006 with neurological signs including limb weakness and circling. Microscopical examination of the brain and spinal cord revealed the presence of non-suppurative encephalitis in all animals. Perivascular cuffing of lymphocytes and macrophages and diffuse gliosis was prominent in the cerebrum and degeneration and/or necrosis of neurons with vacuolation of the neuropil was present in the brainstem. Neuronal necrosis and neuronophagia were noted in the ventral horn of the spinal cord. The distribution of the lesions was closely related to the clinical signs displayed by each calf. Five calves presenting with astasia with low head carriage or torticollis had lesions throughout the central nervous system (CNS). The oldest calf displayed astasia caused by weakness of the "hindlimb" one word and had lesions largely restricted to the caudal spinal cord. Akabane virus (AKAV) antigens were detected immunohistochemically within neurons and axons in lesional tissue. Virus was not isolated from CNS tissue but the AKAV S gene was detected in this tissue from five calves by reverse transcriptase polymerase chain reaction (RT-PCR). It is suggested that AKAV infection is likely to have occurred during the early life period in the calves of this study.
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PMID:Encephalomyelitis of cattle caused by Akabane virus in southern Japan in 2006. 1916 75