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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To define the route of influenza virus invasion into the central nervous system (CNS), an avian influenza A (H5N3) virus was inoculated into mice intranasally or intravenously. Only the intranasal infection group mice showed depression and retention of gas in the digestive system. Pathological findings in the animals were bronchointerstitial pneumonia and non-suppurative encephalitis restricted to the brain stem. The nerve nucleus primarily affected was the nucleus of solitary tract. Prior to the development of the CNS lesions, viral antigen was detected in vagal and trigeminal ganglia. These results suggest that the primarily replicated virus in the respiratory mucosa ascended to the CNS via sensory nerve routes, inducing lesions in the brain stem, and then spread trans-synaptically in the CNS.
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PMID:Avian influenza virus intranasally inoculated infects the central nervous system of mice through the general visceral afferent nerve. 1066 17

Sequence analysis of the hemagglutinin (HA) gene of five Korean H9N2 avian influenza virus (AIV) isolates showed that these viruses were closely related and possibly came from the same source. Phylogenetic analysis of the HA1 subunit of H9 subtype isolates revealed that Korean AIV isolates were different from isolates from the poultry markets in Hong Kong in 1997. None of the Korean AIVs had multiple basic amino acids at the HA cleavage site that confer high pathogenicity to some H5 and H7 AIVs. Phylogenetic analysis of the nucleoprotein and matrix gene demonstrated that Korean isolates cluster with Eurasian origin AIVs. The pathogenic potential of one of the isolates (MS96) was assessed after several passages in 14-day-old embryonated chicken eggs (ECE). Fourteen-day-old ECE derivatives of MS96 showed increased HA titer and embryo mortality in eggs; this was apparent after the third passage in 14-day-old ECE. Sequence analysis of the cleavage site of MS96 after the third and tenth passages in 14-day-old ECE revealed no changes in the amino acid sequence. The pathogenicity of MS96 after the tenth passage in 14-day-old eggs (MS96p10(ECE14)) was tested with 4-wk-old specific-pathogen-free chickens. The 14-day-old derivative, MS96p10(ECE14), showed wider tissue tropism and induced more severe clinical signs than the parent virus. Furthermore, after intranasal inoculation of 86-wk-old broiler breeders and 30-wk-old layers, the MS96p10(ECE14) derivative induced more severe signs of depression than the parent virus as well as a transient drop in egg production.
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PMID:Sequence analysis of the hemagglutinin gene of H9N2 Korean avian influenza viruses and assessment of the pathogenic potential of isolate MS96. 1100 99

Direct bird-to-human transmission, with the production of severe respiratory disease and human mortality, is unique to the Hong Kong-origin H5N1 highly pathogenic avian influenza (HPAI) virus, which was originally isolated from a disease outbreak in chickens. The pathobiology of the A/chicken/Hong Kong/220/97 (H5N1) (HK/220) HPAI virus was investigated in chickens, turkeys, Japanese and Bobwhite quail, guinea fowl, pheasants, and partridges, where it produced 75-100% mortality within 10 days. Depression, mucoid diarrhea, and neurologic dysfunction were common clinical manifestations of disease. Grossly, the most severe and consistent lesions included splenomegaly, pulmonary edema and congestion, and hemorrhages in enteric lymphoid areas, on serosal surfaces, and in skeletal muscle. Histologic lesions were observed in multiple organs and were characterized by exudation, hemorrhage, necrosis, inflammation, or a combination of these features. The lung, heart, brain, spleen, and adrenal glands were the most consistently affected, and viral antigen was most often detected by immunohistochemistry in the parenchyma of these organs. The pathogenesis of infection with the HK/220 HPAI virus in these species was twofold. Early mortality occurring at 1-2 days postinoculation (DPI) corresponded to severe pulmonary edema and congestion and virus localization within the vascular endothelium. Mortality occurring after 2 DPI was related to systemic biochemical imbalance, multiorgan failure, or a combination of these factors. The pathobiologic features were analogous to those experimentally induced with other HPAI viruses in domestic poultry.
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PMID:Pathobiology of A/chicken/Hong Kong/220/97 (H5N1) avian influenza virus in seven gallinaceous species. 1128 Mar 71

Beginning at the end of March 1999, a syndrome characterized by severe depression, anorexia, fever, and respiratory and enteric symptoms appeared in flocks of turkeys and, to a lesser extent, of chickens in the densely populated poultry-rearing regions of northeast Italy. The disease was characterized by sinusitis, tracheitis, peritonitis, and pancreatitis. The mortality varied between 5% and 90%. The disease was diagnosed as low pathogenic avian influenza, H7N1 serotype. After a summer period of declining cases, the disease reappeared in autumn exclusively in turkeys. Since the middle of December 1999, many farms of chickens, turkeys, and guinea fowl were abruptly affected by a highly pathogenic H7N1 virus, with very severe depression and mortality up to 100% in a few days. By the end of March 2000, nearly 500 farms, representing over 15 million birds, were affected or depopulated. To date, control measures have focused on improved biosecurity measures. Vaccine was not allowed, but its use was debated.
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PMID:Avian influenza epidemic in Italy due to serovar H7N1. 1133 92

This investigation assessed the ability of the zoonotic A/chicken/Hong Kong/220/97 (chicken/Hong Kong) (H5N1) highly pathogenic avian influenza virus to infect and cause disease in zebra finches (Taeniopygia guttata), house finches (Carpodacus mexicanus), house sparrows (Passer domesticus), European starlings (Sternus vulgaris), and budgerigars (Melopsittacus undulatus) after intranasal administration. Zebra finches were the most severely affected of the five species, demonstrating anorexia, depression, and 100% mortality within 5 days of inoculation. Gross lesions in this species were absent or only mild. But histologic lesions and the corresponding viral antigen were observed in multiple organs, especially in the nasal cavity, brain, pancreas, spleen, adrenal glands, and ovary. Significant morbidity and mortality also were observed in both house finches and budgerigars. Affected birds of these two species demonstrated anorexia, depression, and neurologic signs and typically were moribund or dead within 2 days of the onset of clinical signs. Gross lesions were mild or absent in house finches and budgerigars. Histologically, the brain and pancreas were the most consistently and severely affected organs in house finches. The brain was the most affected organ in budgerigars. Unlike these three species, house sparrows suffered only mild transient depression, had no mortality, and lacked gross lesions. Viral antigen and microscopic lesions were observed only in the heart and testicle of a minority of birds of this species. Starlings demonstrated neither clinical disease nor mortality and lacked gross and histologic lesions. Viral antigen was not observed in any of the collected tissues from starlings. These results indicate that there is significant variation in the pathogenicity of the chicken/Hong Kong virus for different species of birds, including species within the same order. In addition, neurotropism is a recurrent feature among birds that eventually succumb to infection.
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PMID:Varied pathogenicity of a Hong Kong-origin H5N1 avian influenza virus in four passerine species and budgerigars. 1262 9

The nonpathogenic avian influenza (AI) outbreak in Pennsylvania began in December 1996 when there was a trace back from a New York live bird market to a dealer's flock. A total of 18 commercial layer flocks, two commercial layer pullet flocks, and a commercial meat turkey flock were diagnosed with nonpathogenic AI (H7N2) viral infection with an economic loss estimated at between 3 and 4 million dollars. Clinical histories of flocks infected with the disease included respiratory disease, elevated morbidity and mortality throughout the house, egg production drops, depression, and lethargy. A unique gross lesion in the commercial layers was a severe, transmural oviduct edema with white to gray flocculent purulent material in the lumen. Layer flocks on two separate premises were quarantined but permitted to remain in the facilities until cessation of virus shed was determined through virus isolation. Several months later, clinical AI appeared again in these flocks. It is not known whether the recurrence of disease in these cases is due to persistence of the organism in the birds or the environment. In addition to serologic testing and virologic testing by chicken embryo inoculation, an antigen capture enzyme immunoassay was evaluated as a diagnostic tool for AI. Research projects related to disinfection, burial pits, and geographical system technology were developed because of questions raised concerning transmission, diagnosis, and control of nonpathogenic AI (H7N2).
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PMID:A review of the 1996-98 nonpathogenic H7N2 avian influenza outbreak in Pennsylvania. 1457 71

Seventeen avian species and two mammalian species were intranasally inoculated with the zoonotic A/chicken/Hong Kong/220/97 (chicken/HK) (H5N1) avian influenza (AI) virus in order to ascertain a relative range of susceptible hosts and the pathobiology of the resultant disease. A direct association was demonstrated between viral replication and the severity of disease, with four general gradations being observed among these species. These gradations included the following: 1) widespread dissemination with rapid and high mortality, 2) neurological disease relative to viral neurotropism, 3) asymptomatic infection or only mild transient depression associated with minor viral replication, and 4) absence of disease relative to minimal to no viral replication. This investigation not only demonstrates that the chicken/HK virus could infect multiple avian species, but also that the virulence of the chicken/HK virus varied significantly among avian species, including those species that are members of the same order.
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PMID:Comparative susceptibility of selected avian and mammalian species to a Hong Kong-origin H5N1 high-pathogenicity avian influenza virus. 1457 94

Infections of ostriches with avian influenza A viruses are generally associated with clinical disease, but the occasional high mortality in young birds does not appear to be related directly to virus pathotype. In this study we investigated the pathogenesis of two H7 viruses for 11-wk-old ostriches inoculated intranasally, and clinical symptoms, virus excretion, and immune response were studied. One of the viruses (A/Ostrich/Italy/1038/00) was highly pathogenic for chickens, whereas the other (A/Ostrich/South Africa/1609/91) was of low pathogenicity for chickens. Clinical signs in ostriches receiving virulent virus were slight depression and hemorrhagic diarrhea, while the group receiving avirulent virus was clinically normal except for green diarrhea. Both viruses were transmitted to in-contact sentinel birds housed with the infected groups 3 days postinfection. Postmortem examination of the birds infected (including the sentinel bird) with virus highly pathogenic for chickens were grossly normal except for localized pneumonic lesions. The results of the study are presented and discussed.
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PMID:Pathogenesis of H7 influenza A viruses isolated from ostriches in the homologous host infected experimentally. 1457 32

In March 1999 a syndrome characterized by depression, anorexia, fever, and respiratory and enteric signs appeared in many flocks of turkeys and, to a lesser extent, chickens in the densely populated poultry-rearing regions of Northeastern Italy. Initially the disease was characterized by sinusitis, tracheitis, peritonitis, and pancreatitis. The responsible agent was identified as low-pathogenicity (LP) avian influenza (AI) of H7N1 subtype. Concerning the light layers, the mortality was variable, from 1.7% to 9.5%, whereas egg production decreased by 10% to 40%. According to the epidemiologic data, chickens seemed to be less sensitive to the virus than were turkeys. Nine months later, the AI virus changed to a highly pathogenic (HP) AI virus and affected, besides turkeys, a great number of pullet and layer flocks, with high mortality (80%-100%) in a few days. However, the course of disease was more prolonged in pullets. Within 3 1/2 mo, over 100 outbreaks were reported. Following the HPAI outbreaks, in late 2000 and early 2001, LPAI reemerged, but only one flock of layers was affected.
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PMID:Avian influenza attributable to serovar H7N1 in light layers in Italy. 1457 37

Chickens were intranasally inoculated with Chilean H7N3 avian influenza (AI) viruses of low pathogenicity (LP) (H7N3/LP), high pathogenicity (HP) (H7N3/HP), and a laboratory derivative (02-AI-15-#9) (H7N3/14D) from the LPAI virus to determine pathobiologic effects. All chickens inoculated with H7N3/HP AI virus became infected and abruptly died 2 or 3 days postinoculation, but a few showed moderate depression before death. The H7N3/HP AI virus produced focal hemorrhages of the comb, petechial hemorrhage at the esophageal-proventricular junction and proventricular mucosa, edema and congestion of the lung, petechiation of the spleen, and generalized decrease in body fat. Histologically, severe necrosis, hemorrhage, and inflammation were primarily identified in lungs and the lymphoid tissues. All tissues sampled from the H7N3/HP AI group were positive for the AI viral antigen, predominantly in endothelium of blood vessels throughout most tissues and less frequently in histiocytes and cellular debris of lymphoid tissues. Even less consistently, cardiac myocytes, hepatocytes, Kupffer cells, glandular epithelial cells, microglial cells, and neurons became infected. These studies suggest the Chilean H7N3/LP AI virus was poorly infectious for chickens and may have been recently introduced from a nongalliform host. By contrast, the H7N3/HP AI virus was highly infectious and lethal for chickens. The H7N3/HP AI virus had a strong tropism for the cardiovascular system, principally vascular endothelium, which is similar to the viral tropism demonstrated previously with other H5 and H7 HPAI viruses. Interestingly, the H7N3/LP AI virus on intravenous inoculation replicated in cardiac myocytes, a feature of HPAI and not LPAI viruses, which further supports the theory that the H7N3/LP AI virus was in transition from LP to HP.
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PMID:Comparative pathobiology of low and high pathogenicity H7N3 Chilean avian influenza viruses in chickens. 1507 5


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