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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Specific-pathogen-free laying hens were inoculated with avian influenza virus (AIV) A/chicken/Alabama/7395/75 (H4N8) either intratracheally (IT) or intravenously (IV). IT inoculation produced a localized infection of the upper and lower respiratory tracts with lesions of tracheitis, bronchitis, airsacculitis, and pneumonia around the secondary bronchi. IV inoculation produced a systemic infection with major lesions of nephritis, interstitial pneumonia, salpingitis, and splenic and hepatic necrosis. In IV-inoculated hens, AIV nucleo-protein was demonstrated within renal tubule epithelium, in luminal surface and glandular oviduct epithelium, and in mononuclear cells within pulmonary blood capillaries. However, no virus was recovered from internal contents of eggs laid between days 1.5 and 5 postinfection. These data indicate that A/chicken/Alabama/7395/75 has tissue tropism and pathogenicity for the respiratory and urogenital systems of reproductively active laying hens. Site and severity of lesion development are determined by the localized or systemic nature of AIV infection.
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PMID:Pathological studies of A/chicken/Alabama/7395/75 (H4N8) influenza virus in specific-pathogen-free laying hens. 800 96

We compared two strains of avian influenza A viruses of subtype H10 by exposing mink to aerosols of A/mink/Sweden/3,900/84 (H10N4) naturally pathogenic for mink, or A/chicken/Germany/N/49, (H10N7). Lesions in the respiratory tract during the first week after infection were studied and described. Both virus strains caused inflammatory reactions in the lungs and antibody production in exposed mink but only mink/84 virus was reisolated. The lesions caused by mink/84 virus were more severe with higher area density of pneumonia, lower daily weight gain, and more virus in the tissues detected by immunohistochemistry. The results indicate that mink/84 (H10N4), but not chicken/49 virus (H10N7), established multiple cycle replication in infected cells in the mink.
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PMID:Two avian H10 influenza A virus strains with different pathogenicity for mink (Mustela vison). 963 39

The transmission of avian H5N1 influenza viruses to 18 humans in Hong Kong in 1997 with six deaths established that avian influenza viruses can transmit to and cause lethal infection in humans. This report characterizes the antigenic and biological properties of the H5N1 influenza viruses isolated from chickens, ducks, and geese from farms and poultry markets in Hong Kong during 1997 and compares them with those of virus isolated from the index human case. Each of the H5N1 viruses from Hong Kong poultry markets that were tested were lethal in chickens, possessed polybasic amino acids at the carboxy-terminus of HA1, and by definition were highly pathogenic in poultry. The available nonpathogenic H5 influenza viruses and the pathogenic H5N1 virus from Hong Kong were analyzed with monoclonal antibodies prepared to A/chicken/Pennsylvania/1370/83 (H5N2). The analysis revealed limited antigenic drift in 15 years and established that monoclonal antibodies are useful reagents for identification and antigenic analysis of avian strains that may transmit to humans in the future. One of the monoclonal antibodies permitted separation of the H5N1 influenza viruses from poultry into two groups that correlated with the presence or absence of a carbohydrate at residue 158 adjacent to the receptor binding site on HA. The H5N1 viruses examined replicated in geese, pigs, rats, and mice, but to only a very limited extent in ducks. It is noteworthy that all infected geese shed virus and that the H5N1 viruses caused disease signs and death in a portion (3 of 16) of the geese, with evidence of systemic spread to the brain. The tropism for geese is unusual and may provide insight into the origin of these viruses. In mice, the H5N1 virus caused lethal pneumonia and spread systemically to the brain. Mice would thus provide an ideal model system for studying immune responses and pathogenesis. Transmission experiments in chickens revealed that the H5N1 viruses are spread by fecal-oral transmission rather than by aerosol, and that the viruses are inactivated by drying of feces at ambient temperature. However, infectivity is maintained for at least 4 days in wet feces at 25 degreesC. There were differences in the morphology of the H5N1 viruses isolated from birds and humans. The perpetuation of H5N1 influenza viruses in the poultry markets in Hong Kong and the transmission of these viruses to humans emphasize the importance of these markets in the epidemiology of influenza. The poultry markets are of critical importance in the perpetuation and transmission of influenza viruses to other avian species and to mammals, including humans.
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PMID:Characterization of avian H5N1 influenza viruses from poultry in Hong Kong. 987 12

Avian influenza virus was not known to cause systemic infection in humans before. We report a 3-year-old boy with good past health who developed pneumonia caused by H5N1 avian influenza A virus (A/Hong Kong/156/97). The virus was isolated from a tracheal aspirate. There were complications of Reye's syndrome, adult respiratory distress syndrome, and multiple organ system failure. He had a history of receiving aspirin. His adult respiratory distress syndrome did not respond to endotracheal surfactant replacement therapy. He died 6 days after admission. Clinicians should be alert to the importance of a new human influenza strain.
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PMID:The first case of H5N1 avian influenza infection in a human with complications of adult respiratory distress syndrome and Reye's syndrome. 1036 63

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

Human influenza viruses manage to cause epidemics almost every year. The circulating viruses change their surface glycoproteins by accumulating mutations (antigenic drift) which results in variant viruses of the same subtype that are able to evade the immune pressure in the population. Every now and then, a completely new subtype of influenza A virus is introduced in the human population, which can result in an influenza pandemic. Pandemic human influenza viruses have been emerging for many centuries. Based on the genetic information of influenza viruses that have been isolated in this century, introduction of genes of the avian influenza virus reservoir obviously is required. Interspecies transmission, via another mammalian host and reassortment of avian and human influenza viruses are potential mechanisms for such an introduction. A summary of the cases in which influenza viruses containing avian-like gene segments were introduced into the human population is presented. In three cases, such infections resulted in conjunctivitis. Influenza-like illness and even pneumonia was reported in some other infections. Finally, a mortality rate of 33% was observed in the avian influenza A (H5N1) viruses that infected 18 people in Hong Kong in 1997. Although some of these viruses fulfilled some criteria of pandemic influenza viruses, they lacked the ability to rapidly spread through the human population.
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PMID:Pandemic influenza is a zoonosis, as it requires introduction of avian-like gene segments in the human population. 1079 85

In October 1999, H4N6 influenza A viruses were isolated from pigs with pneumonia on a commercial swine farm in Canada. Phylogenetic analyses of the sequences of all eight viral RNA segments demonstrated that these are wholly avian influenza viruses of the North American lineage. To our knowledge, this is the first report of interspecies transmission of an avian H4 influenza virus to domestic pigs under natural conditions.
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PMID:Isolation and characterization of H4N6 avian influenza viruses from pigs with pneumonia in Canada. 1098 81

It is generally believed that pigs can serve as an intermediate host for the transmission of avian influenza viruses to humans or as mixing vessels for the generation of avian-human reassortant viruses. Here we describe the antigenic and genetic characterization of two influenza A (H1N1) viruses, which were isolated in The Netherlands from two patients who suffered from pneumonia. Both viruses proved to be antigenically and genetically similar to avian-like swine influenza A (H1N1) viruses which currently circulate in European pigs. It is concluded that European swine H1N1 viruses can infect humans directly, causing serious disease without the need for any reassortment event.
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PMID:Antigenic and genetic characterization of swine influenza A (H1N1) viruses isolated from pneumonia patients in The Netherlands. 1128 12

The first outbreak of avian influenza A(H5N1) virus in humans occurred in Hong Kong in 1997. Infection was confirmed in 18 individuals, 6 of whom died. Infections were acquired by humans directly from chickens, without the involvement of an intermediate host. The outbreak was halted by a territory-wide slaughter of more than 1.5 million chickens at the end of December 1997. The clinical spectrum of H5N1 infection ranges from asymptomatic infection to fatal pneumonitis and multiple organ failure. Reactive hemophagocytic syndrome was the most characteristic pathologic finding and might have contributed to the lymphopenia, liver dysfunction, and abnormal clotting profiles that were observed among patients with severe infection. Rapid diagnosis with the use of reverse-transcription polymerase chain reaction and monoclonal antibody-based immunofluorescent assay were of great clinical value in the management of the outbreak. The experience of the H5N1 outbreak in Hong Kong underscores the importance of continuous surveillance of influenza virus strains in humans and in other animal species.
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PMID:Outbreak of avian influenza A(H5N1) virus infection in Hong Kong in 1997. 1193 98

The outbreak of avian influenza A due to an H7N7 virus in Dutch poultry farms turned out to have public-health effects for those who were involved in the management of the epidemic and who were thus extensively exposed to contaminated excreta and dust. An outbreak-management team (OMT) of experts in virology, infectious diseases and public health advised the Dutch government with respect to the potential health effects on humans. Strict hygiene measures were advised. Moreover, vaccination against human influenza was advised to prevent emergence of a new pandemic virus in humans. Since the human influenza virus H3N2 circulated at the same time, a double infection and emergence of a new human virus was the main fear on which prevention was focused. Conjunctivitis was observed in about 10% of the people involved. The conjunctivitis was sometimes accompanied by mild flu-like symptoms and incidental transmission between humans occurred as well. Because of the unexpected high incidence of symptomatic infections, proven to be caused by the H7N7 strain, oseltamivir was advised as an additional control measure, both for the treatment of symptoms and prophylactically for those with prolonged occupational exposure. After the unfortunate death of a veterinarian due to pneumonia caused by the avian virus, the preventive policy was further extended to people with short and incidental exposure to infected flocks. It is concluded that the policy was adequate, in spite of the unforeseen victim.
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PMID:[Avian influenza and oseltamivir; a retrospective view]. 1296 35


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