Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The scientific literature of the past century is reviewed on fowl plague (presently termed highly pathogenic avian influenza, HPAI) in pigeons. HPAI viruses cause epidemic disease outbreaks with high rates of losses in many avian species, particularily in chickens and turkeys. Also susceptible to disease are quails, guinea fowl, ducks, geese, ostriches, passerine birds, and birds of prey whereas conflicting reports on the susceptibility of the domestic pigeon exist. Based on literature reports and on own experiments, and applying as criteria for judgements clinically overt forms of disease, virus multiplication plus shedding and seroconversion, it is concluded that domestic pigeons are only partially susceptible to influenza A viruses of the haemagglutinin subtype H7. Infection of pigeons with H7 viruses results only in some of them in signs, virus shedding and seroconversion. Using the same criteria, pigeons appear to be even less susceptible to infection with influenza A viruses of the H5 subtype. Only one of five publications describe in 1/19 pigeons exposed to H5 influenza A virus depression one day before death, and only 2/19 multiplied and excreted virus, and 1/19 developed circulating antibodies. Consequently, pigeons play only a minor role in the epidemiology of H5 influenza viruses. In contrast, following infection with influenza A virus of the subtype H7 clinical signs in pigeons consist of conjunctivitis, tremor, paresis of wings and legs, and wet droppings. H7-infected pigeons multiply and excrete H7 viruses and develop circulating antibodies. Albeit of the status of infection, free-flying domestic pigeons can act as mechanical vectors and vehicles for long-distance transmission of any influenza A virus if plumage or feet were contaminated.
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PMID:Review of the literature on avian influenza A viruses in pigeons and experimental studies on the susceptibility of domestic pigeons to influenza A viruses of the haemagglutinin subtype H7. 1564 16

The present study reports the clinical, virological and pathological findings observed in a natural outbreak of highly pathogenic avian influenza in farmed commercial ducks. The ducks developed clinical signs, including mild respiratory distress, depression, mild diarrhoea, loss of appetite and increasing mortality (up to 12%). At necropsy, multifocal mottled necrosis was commonly found in the pancreas with splenomegaly, hepatomegaly, and swollen kidneys. Microscopically, there was necrotized pancreatitis and hepatitis, and lymphocytic meningoencephalitis and myocarditis. Influenza viral antigen was demonstrated in areas closely associated with histopathological lesion. Avian influenza virus was isolated from the caecal tonsil, faeces, and kidney of the domestic ducks. The isolated virus was identified as a highly pathogenic H5N1, with a haemagglutinin proteolytic cleavage site deduced amino acid sequence of ... QREKRKKR/GLFGAIAG ... In order to determine the pathogenicity of the isolate, eight 6-week-old specific pathogen free chickens were inoculated intravenously with the virus, and all birds died within 24 h after inoculation. This is the first report of an outbreak of highly pathogenic avian influenza with clinical signs in commercial domestic ducks in South Korea.
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PMID:Highly pathogenic avian influenza (H5N1) in the commercial domestic ducks of South Korea. 1614 75

To investigate the mechanism of avian influenza outbreak wildly in water fowls, the co-pathogens, especially that caused immuno-depression were studied. A pair of degenerated primers, which amplified a fragment of 552bp in length, was designed and synthesized based on the published goose and other Circovirus sequences. The specific PCR product was amplified from the goose sample of Yongkang avian influenza case of Zhejiang Province. The fragment was then sequenced and the result showed the existence of the GoCV. The opposite part of the genome was further amplified using inverse primers designed based on the 552bp sequence obtained and the 1821bp full length genomic sequence of GoCV-yk01 was compiled using Seqman program of DNAStar. Sequence analysis showed that the GoCV-yk01 possessed common features of circovirus included potential replication associated stem-loop structure and the Rep protein motifs. Homology analysis showed that the sequence of GoCV-yk01 had 91% approximately 93% similarity to that of Taiwan and Germany strains. Phylogenetic analysis with ClustalW, however, showed that the GoCV-yk01 was on a different branch away from Taiwan and Germany strains. Circovirus usually causes immuno-depression and results in secondary infection, as it infects rapid growing cells as lymphocyte. It is speculated that the infection of GoCV may be a part of the reason of the avian influenza outbreak of the Yongkang case. The GoCV-yk01 is the first GoCV strain reported in mainland of China.
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PMID:[Cloning and analysis of the complete genome of a Goose circovirus from Yongkang Zhejiang]. 1649 92

This investigation assessed the susceptibility of experimentally infected pigeons to the highly pathogenic avian influenza virus (HPAIV) H5N1 that caused recent outbreaks of avian influenza in birds and humans in several countries of Asia. For this purpose 14 pigeons were infected ocularly and nasally with 10(8) EID50 and clinical signs were recorded and compared with five chickens infected simultaneously as positive controls. The chickens demonstrated anorexia, depression, and 100% mortality within 2 days postinoculation. Three of the pigeons died after a history of depression and severe neurological signs consisting of paresis to paralysis, mild enteric hemorrhage, resulting in a mortality of 21%. Gross lesions in these pigeons were mild and inconsistent. Occasionally subcutaneous hyperemia and hemorrhage and cerebral malacia were observed. Microscopic lesions and detection of viral antigen were confined to the central nervous system of these pigeons. In the cerebrum and to a minor extent in the brain stem a lymphohistiocytic meningoencephalitis with disseminated neuronal and glial cell necrosis, perivascular cuffing, glial nodules, and in one bird focally extensive liquefactive necrosis could be observed. The remaining nine pigeons showed neither clinical signs nor gross or histological lesions associated with avian influenza, although seroconversion against H5 indicated that they had been infected. These results confirm that pigeons are susceptible to HPAIV A/chicken/Indonesia/2003 (H5N1) and that the disease is associated with the neurotropism of this virus. Although sentinel chickens and most pigeons did not develop disease, further experiments have to elucidate whether or not Columbiformes are involved in transmission and spread of highly pathogenic avian influenza.
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PMID:Neurotropism of highly pathogenic avian influenza virus A/chicken/Indonesia/2003 (H5N1) in experimentally infected pigeons (Columbia livia f. domestica). 1684 88

Low pathogenic avian influenza subtype H9N8 was diagnosed on a Korean native chicken farm in Gyeonggi province, South Korea, in late April 2004. Clinical signs included moderate respiratory distress, depression, mild diarrhoea, loss of appetite and a slightly elevated mortality (1.4% in 5 days). Pathologically, mucopurulent tracheitis and air sacculitis were prominently found with urate renal deposition. The isolated A/chicken/Kr/164/04 (H9N8) had an Ala-Ser-Gly-Arg (A/S/G/R) motif at the cleavage site of haemagglutinin, which has been commonly found in H9N2 isolated from Korean poultry. Phylogenetic analysis of the haemagglutinin and neuraminidase genes of the H9N8 avian influenza virus (AIV) isolate showed that reassortment had occurred. Its haemagglutinin gene was similar to that of Korean H9N2 AIVs, but its neuraminidase gene was closely related to that of A/WBF/Kr/KCA16/03 (H3N8) isolated from the faeces of wild birds in Korea. The pathogenicity of the isolate was tested on 6-week-old specific pathogen free chickens. The inoculated virus (H9N8) was recovered from most tested organs, including the trachea, lung, kidney, spleen, and caecal tonsil. This is the first report of an outbreak of low pathogenic avian influenza in chickens caused by AIV subtype H9N8.
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PMID:An outbreak of avian influenza subtype H9N8 among chickens in South Korea. 1712 32

To assess the potential of quail as an intermediate host of avian influenza, we tested the influenza A/Mallard/ Potsdam/178-4/83 (H2N2) virus to determine whether through adaptation a mallard strain can replicate and transmit in quail, as well as other terrestrial birds. After five serial passages of lung homogenate a virus arose that replicated and transmitted directly to contact cage mates. To test whether adaptation in quail led to interspecies transmission, white leghorn chickens were infected with the wild-type (mall/178) and quail-adapted (qa-mall/178) viruses. The results show that mall/178 H2N2 does not establish an infection in chickens nor does it transmit, while qa-mall/178 H2N2 infects and transmits to contact chickens causing clinical signs like depression and diarrhea. Completed sequences indicate six amino acid changes spanning four genes, PB2, PB1, HA, and NP, suggesting that the internal genes play a role in host adaptation. Further adaptation of qa-mall/178 in white leghorn chickens created a virus that replicated more efficiently in the upper and lower respiratory tract. Sequence analysis of the chicken-adapted virus points to a deletion in the neuraminidase stalk region.
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PMID:Adaptation of influenza A/Mallard/Potsdam/178-4/83 H2N2 virus in Japanese quail leads to infection and transmission in chickens. 1749 63

Clinical signs, serologic response, viral contents of the trachea and intestine, and histopathological and ultrastructural changes of the tracheal epithelium of Japanese quail experimentally infected with field isolate of H9N2 avian influenza were studied. Vaccinated and unvaccinated quail were inoculated with 10(6.3) 50% embryo infectious dose/bird of A/ chicken/Iran/SH-110/99 (H9N2) virus via nasal inoculation. Clinical signs such as depression, ruffled feathers, diarrhea, and nasal and eye discharges were observed 6 days postinfection (PI). No mortality was observed; however, there was reduction in feed and water consumption and egg production. However, the serologic response of vaccinated challenged and unvaccinated challenged birds was not significantly different. Unvaccinated challenged quail showed more severe histopathologic reaction in their lungs and trachea. Hyperemia, edema, infiltration of inflammatory cells, and deciliation and sloughing of the tracheal epithelium were observed. Ultrastructural study showed dilatation of endoplasmic reticulum and degeneration of Golgi apparatus and cilia of the tracheal lining cells of respiratory epithelium.
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PMID:Pathobiology of H9N2 avian influenza virus in Japanese quail (Coturnix coturnix japonica). 1749 91

The ongoing H5N1 Asian epidemic is currently affecting a number of avian species including ducks. These birds are an important part of the poultry industry in the affected countries, and it is likely that they are acting as a reservoir of infection. Ten Pekin ducks were challenged with 100 microl containing 10(7) 50% egg infective dose of the highly pathogenic avian influenza virus (HPAIV) A/Duck/Vietnam/12/05 (H5N1), administered by an intra-nasal and oral route. Clinical symptoms were recorded twice a day up to 14 days postinfection (dpi). Clinical signs were first noted at 2 dpi, with conjunctivitis and slight depression, and progressed over a period of 1-3 days to severe neurologic signs consisting of torticollis, incoordination, tremors, and seizures. Survival times varied from 3 to 7 dpi. On postmortem examination, hemorrhages were observed in the duodenum, ceca, proventriculus, ventriculus, trachea, pancreas, and brain. Histologic lesions, as well as immunohistochemistry positivity, were recorded in the pancreas and brain. In situ hybridization revealed viral antigen associated with acinar pancreatic cells, bronchial epithelial cells, and with cells of the central nervous system as well as neurons of the submucosal plexus of the duodenum. Our experimental findings agree with those previously observed in ducks naturally infected with HPAIV H5N1 viruses, confirming the acquired viral neurotropism and pancreatotropism, as previously noted in other avian species, as well as in humans.
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PMID:Pathologic findings of highly pathogenic avian influenza virus A/Duck/Vietnam/12/05 (H5N1) in experimentally infected pekin ducks, based on immunohistochemistry and in situ hybridization. 1784 35

Although cats had been considered resistant to disease from influenza virus infection, domestic cats and large felids are now known to be naturally und experimentally susceptible to infection with highly pathogenic avian influenza virus H5N1 (HPAIV H5N1). The virus causes systemic infection, lung and liver being the mainly affected organs. Infected cats show fever, depression, dyspnoea, and neurological signs, but subclinical infections have also occurred. Mostly, cats have been infected by direct contact with affected birds, especially by eating raw poultry; transmission from cat to cat may also occur. Little is known about the role of cats in the epidemiology of the virus. So far, no reassortment between avian and mammalian influenza viruses has occurred in cats, but experts fear that cats might give the virus an opportunity to adapt to mammals. This publication gives a review on avian influenza in cats with a focus on practical aspects for veterinarians.
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PMID:Avian influenza A H5N1 infections in cats. 1861 84

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


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