Pathology and Pathogenesis
Acland, H.M., R.J. Eckroade, and L.A. Bachin. (1984). Lesions in chickens involved in the outbreak of highly pathogenic avian influenza in Pennsylvania 1983-84. [Abstract]. In: 35th Annual Meeting of the American College of Veterinary Pathologists, p. 83.
NAL Call Number: SF769.A54
Descriptors: avian influenza virus, lesions, outbreaks, chickens, Pennsylvania, abstract.
Acland, H.M., L.A. Silverman Bachin, and R.J. Eckroade (1984). Lesions in broiler and layer chickens in an outbreak of highly pathogenic avian influenza virus infection. Veterinary Pathology 21(6): 564-9. ISSN: 0300-9858.
NAL Call Number: 41.8 P27
Abstract: Fifteen chickens, five broilers and ten layers, from the Pennsylvania 1983 outbreak of highly pathogenic avian influenza virus infection, were examined. Gross lesions in the broilers were limited to serosal petechiae and dehydration. In the layers there was comb edema, vesiculation, and necrosis. Microscopic lesions were mild to severe diffuse nonsuppurative encephalitis, very mild to severe diffuse necrotizing pancreatitis, and very mild to severe subacute necrotizing myositis involving numerous skeletal muscles and most severe in the external ocular muscles and limbs. While many of these lesions have been seen in experimental infections of chickens with influenza viruses, the pattern of organs involved in this group of chickens is distinctive.
Descriptors: chickens, disease outbreaks veterinary, fowl plague pathology, brain pathology, fowl plague epidemiology, inclusion bodies, viral ultrastructure, muscles pathology, myocardium pathology, pancreas pathology, pancreas ultrastructure, Pennsylvania, proventriculus pathology.
Afzal, M., A.H. Cheema, and Khalid Naeem (2000). Pathogenicity of avian influenza virus strain H7N3in chicken. Pakistan Veterinary Journal 20(3): 139-141. ISSN: 0253-8318.
NAL Call Number: SF604.P32
Descriptors: experimental infection, histopathology, clinical signs, lesions, mortality, avian influenza virus, Gallus gallus, Phasianidae, Galliformes, Pakistan.
Alexander, D.J., W.H. Allan, D.G. Parsons, and G. Parsons (1978). The pathogenicity of four avian influenza viruses for fowls, turkeys and ducks. Research in Veterinary Science 24(2): 242-7. ISSN: 0034-5288.
NAL Call Number: 41.8 R312
Abstract: Groups of 10 two-week-old chicks, turkey poults and ducklings were each infected by the intranasal route with one of four avian influenza viruses: a/fowl/Germany/34 (Hav 1N))--Rostock, A/FPV/Dutch/27 (Hav 1 Neq 1)--Dutch, A/fowl/Victoria/75 (Hav 1 Neq 1)--Australian, and A/parrot/Ulster/73 (Hav 1 N1)--Ulster. Eight hours after infection 10 birds of the same age and species were placed in contact with each group and allowed to mix. The clinical signs of disease and onset of sickness and death were recorded. Ulster virus was completely avirulent for all birds. Rostock, Dutch and Australian viruses were virulent for fowls and turkeys causing death in all birds with the exception of 3/10 in contact fowls from the Rostock virus group and 2/10 in contact fowls from the Australian virus group. Only Rostock virus caused sicked sickness or death in ducks, 9/10 intranasally infected and 6/7 in contact birds showed clinical signs and 2/10 intranasally infected and 3/7 in contact ducks died. Intranasal and in contact pathogenicity indices were calculated for each virus in each bird species and indicated quantitatively the differences in virulence of the four virus strains. Virus isolation and immune response studies indicated that surviving in contact fowls in the Rostock virus group had never been infected but that surviving Australian virus in contact fowls had recovered from infection. Infection was not established in Ulster virus in contact fowls and Australian virus intranasally infected and in contact ducks. The birds in all other groups showed positive virus isolations and a high incidence of positive immune response. The last virus isolation was made at 22 days after intranasal infection of ducks with Ulster virus.
Descriptors: chickens, ducks, fowl plague etiology, influenza A virus avian pathogenicity, turkeys, antibodies, viral analysis, fowl plague immunology, fowl plague microbiology, avian immunology, virulence.
Berry, D.M. (1969). Pathogenicity of avian influenza A viruses. Proceedings of the Royal Society of Medicine 62(1): 45-6. ISSN: 0035-9157.
NAL Call Number: 448.9 R814
Descriptors: orthomyxoviridae pathogenicity, poultry diseases etiology, chickens, eggs, Mycoplasma infections complications, poultry diseases diagnosis, serologic tests.
Brown, C.C., H.J. Olander, and D.A. Senne (1992). A pathogenesis study of highly pathogenic avian influenza virus H5N2 in chickens, using immunohistochemistry. Journal of Comparative Pathology 107(3): 341-8. ISSN: 0021-9975.
NAL Call Number: 41.8 J82
Abstract: Eighteen specific pathogen-free chickens (nine hens older than 1 year and nine 15-week-old males) were inoculated with highly pathogenic avian influenza virus A/Chicken/Pennsylvania/1370/1983 (H5N2). Birds were serially killed and tissues collected for histological and immunohistochemical evaluation. In the group of older hens, disease was acute or peracute. By immunohistochemistry, antigen was abundant in capillary endothelium in multiple organs, and staining for antigen in parenchymal cells was marked in brain and heart. In the group of younger male birds, disease was subacute. Immunohistochemical staining of capillary endothelium was less pronounced and viral antigen staining was evident in the parenchymal cells of the heart, brain and kidney.
Descriptors: antigens, viral analysis, brain immunology, endothelium, vascular immunology, fowl plague pathology, influenza A virus avian pathogenicity, myocardium immunology, chickens, fowl plague immunology, immunohistochemistry, avian classification.
Brugh, M. (1988). Highly pathogenic virus recovered from chickens infected with mildly pathogenic 1986 isolates of H5N2 avian influenza virus. Avian Diseases 32(4): 695-703. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: A combination of in vitro and in vivo selection procedures was used to examine the possibility that certain mildly pathogenic field isolates of avian influenza (AI) virus may contain minority subpopulations of highly pathogenic virus. Two mildly pathogenic H5N2 isolates, A/chicken/New Jersey/12508/86 (NJ12508) and A/chicken/Florida/27716/86 (FL27716), recovered from chickens epidemiologically associated with urban live-bird markets, were cloned in trypsin-free chicken embryo fibroblast cultures. Selected clones were inoculated intranasally and intratracheally (IN/IT) into specific-pathogen-free laying hens, and virus reisolated from the hens that died was serially passed in hens by IN/IT inoculation. Several highly pathogenic reisolates were recovered from hens infected with the cloned NJ12508 or FL27716 virus. A highly pathogenic NJ12508 reisolate killed 19 of 24 IN/IT-inoculated hens, and a FL27716 reisolate killed all 24 inoculated hens; signs and lesions were typical of fowl plague. In contrast, uncloned NJ12508 stock virus killed 1 of 24 hens and FL27716 stock virus killed 4 of 24 hens, and neither produced the complete spectrum of lesions associated with fowl plague. Recovery of highly pathogenic viruses from these isolates demonstrates the coexistence of pathogenically distinct subpopulations of virus. Competition for dominance among such subpopulations could explain the variable pathogenicity of some AI viruses.
Descriptors: chickens microbiology, influenza A virus avian pathogenicity, cultured cells, cytopathogenic effect, viral, fowl plague microbiology, fowl plague mortality, avian isolation and purification, serial passage, species specificity, trypsin diagnostic use.
Brugh, M. (1996). Pathogenicity of three avian influenza viruses for leghorn hens of difference ages. Avian Diseases 40(3): 725-728. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Pronounced host effects on clinical responses to influenza virus infection were not observed in any of seven trials in which young (26-43 weeks) and old (65-94 weeks) leghorn hens were inoculated with low pathogenic subtype H5N2, H4N8, or H3N2 virus. In two of seven trials, where hens were infected with H4N8 or H3N2 virus, morbidity rates were slightly higher for old hens than for young hens. These observations indicate that host age effects on the severity of uncomplicated influenza virus infections are likely to be minimal in sexually mature chickens.
Descriptors: chickens, females, avian influenza virus, pathogenicity, age, morbidity, mortality, symptoms, maturity, biological properties, birds, developmental stages, domestic animals, domesticated birds, epidemiology, Galliformes, influenza virus, livestock, microbial properties, orthomyxoviridae, poultry, sex, useful animals, viruses, age differences, maturity stage.
Brugh, M. (1992). Re-evaluation of the pathogenicity of A/chicken/Alabama/75 (H4N8) influenza virus. Avian Diseases 36(4): 968-974. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Avian influenza (AI) virus A/chicken/Alabama/7395/75 (H4N8), a putatively non-pathogenic virus associated with a self-limiting outbreak of severe disease in commercial layers, was selectively passed in chickens or in cell cultures and then in chickens to determine whether virus with increased pathogenicity would emerge. When 20 derivatives of the parental virus were each inoculated intranasally and intratracheally in leghorn hens, mortality rates ranged from zero (0/24) to 25% (6/24); mortality was 4% (1/24) for hens inoculated with the parental virus. Many virus reisolates (51/144) from hens that died exhibited high pathogenicity, killing at least six of eight intravenously inoculated 4-week-old chickens. Most derivatives examined produced plaques in trypsin-free cell cultures more efficiently than the parental virus, but the highest plaquing efficiencies observed (10%) were lower than would be expected (100%) for highly pathogenic subtype H5 or H7 AI viruses. These results confirm that the Alabama H4N8 virus can acquire increased pathogenicity upon passage in chickens and suggest that it may have acted alone in producing the severe disease observed in laying chickens in Alabama.
Descriptors: chickens, avian influenza virus, pathogenicity, cell culture, mortality, biological properties, birds, culture techniques, domestic animals, domesticated birds, Galliformes, in vitro culture, influenza virus, livestock, microbial properties, poultry, useful animals, viruses.
Capua, I., C. Casaccia, C. Pompilii, S. Olivieri, and M. Ianniello (1998). Ricerca di anticorpi nei confronti di patogeni aviari in struzzi (Struthio camelus) di importazione. [Serological investigation for avian pathogens in imported ostriches (Struthio camelus)]. [36. Meeting of Italian Society of Poultry Pathology on new aspects of vaccine prophylaxis in aviculture]. Forli (Italy). 25-26 Sep 1997. Selezione Veterinaria (Italy). (8-9): 655-659.
NAL Call Number: 241.71 B75
Abstract: An investigation was carried out on 700 sera obtained from imported ostriches between 1994 and 1997 for the detection of antibodies against selected viral and bacterial avian pathogens. Sera were tested for antibodies against Newcastle disease, avian influenza and Crimean-Congo haemorrhagic fever (CCHF), according to OM 6/6/1992 and 24/10/1992. Sera were also processed for the detection of antibodies against PMV3, PMV6, IBV, EDS'76, TRT, HEV, IBD and S. enteritidis. All samples were negative for NDV, influenza and CCHF. Low positivities were detected for other viral antigens, while a high prevalence was recorded for S. enteritidis.
Descriptors: ostriches, antibodies, Salmonella enteritidis, animal health, legislation, Italy, disease surveillance, introduced breeds, disease surveys, immunological techniques, blood serum, Newcastle disease, avian influenza virus, paramyxovirus aviare, avian infectious bronchitis virus, enteritis, rhinotracheitis, animal viruses, bacteria, birds, blood, breeds animals, coronaviridae, digestive system diseases, enterobacteriaceae, epidemiology, Europe, immunological factors, infectious diseases, influenza virus, intestinal diseases, organic diseases, orthomyxoviridae, respiratory diseases, Salmonella, Struthioniformes, surveys, taxa, viroses, viruses, Western Europe.
Capua, I., F. Mutinelli, M.A. Bozza, C. Terregino, and G. Cattoli (2000). Highly pathogenic avian influenza (H7N1) in ostriches (Struthio camelus). Avian Pathology 29(6): 643-646. ISSN: 0307-9457.
NAL Call Number: SF995.A1A9
Abstract: The clinical, virological and pathological findings observed in a natural outbreak of highly pathogenic avian influenza in intensively farmed ostriches (Struthio camelus) are reported. Clinical signs characterized by anorexia, depression, nervous and enteric signs were observed in young birds, which resulted in death of 30% of the affected birds. Virus isolation performed in accordance with the guidelines listed in European Union Directive 92/40/EEC yielded an influenza A virus of the H7N1 subtype with a deduced cleavage site motif containing multiple basic amino acids, typical of highly pathogenic viruses. Gross lesions, mainly haemorrhagic enteritis and liver degeneration and necrosis, were confirmed by histopathology and immunohistochemistry, resulting in the detection of necrotic lesions and influenza A nucleoprotein in selected organs. The findings reported indicate that ostriches are susceptible to highly pathogenic avian influenza.
Descriptors: animal husbandry, infection, respiratory system, anorexia nervosa, behavioral and mental disorders, avian influenza A, natural outbreak, respiratory system disease, viral disease, depression, behavioral and mental disorders, hemorrhagic enteritis, vascular disease, histopathological analysis analytical method, immunohistochemistry, immunohistochemical, immunocytochemical techniques, analytical method, European Union Directive 92 40 EEC, guidelines, death, necrosis, ostrich farming, case study.
Casaubon Hugening, M.T., A. Hernandez Magdaleno, J. Garcia Garcia, and M.L. Rosales M. (1996). Lesiones cutaneas causadas por el virus de influenza aviar A/Ck / Queretaro / 14588-619 / 95 (H5 N2) altamente patogeno. [Skin lesions caused by highly pathogenic avian influenza virus A/Ck / Queretaro / 14588-619 / 95 (H5 N2)]. In: Reunion Nacional de Investigacion Pecuaria, Cuernavaca, Morelos, (Mexico), p. 91.
Abstract: Se plantearon 2 hipotesis referentes a la posible patogenia de dichas lesiones, y se llevo a cabo un estudio morfologico preliminar, al respecto. En el CENID Microbiologia, se inocularon 16 aves, 8 Indian River de 7 semanas de edad y 8 Leghorn de 4 semanas de edad, instilando 0.2ml de liquido alantoideo por via intravenosa y 1ml traqueal, con virus de la cepa A/Ck/Queretaro/14588-619/95 (H5 N2) Alta patogenicidad (!06 DLP 50% 3 semanas/ml de liquido alantoideo). La toma de muestras para histopatologia y microscopia electronica de llevaron a cabo a los 8 dias postinoculacion en los pollos de engorda y a los 5 dias los Leghorn. La morfopatologia macroscopica y microscopica de las lesiones cutaneas resultaron ser mas severas en los pollos de engorda que en las aves Leghorn, encontrandose en los primeros: blefaritis serohemorragica severa con focos de necrosis. El epitelio de las barbillas, cresta, region esternal, metatarsos, dedos y cojinete plantar se encontro muy tumefacto debido a acumulo de abundante exudado serohemorragico en tejido subcutaneo, cianotico y con varias areas de necrosis de la epidermis que sufria descamacion mientras que, en las aves Leghorn no se apreciaron areas de necrosis en epidermis y la tumefaccion fue moderada. En el estudio microscopico de los cortes de epitelio fue sorprendente la gran cantidad de pigmento de origen hematico disperso en todo el corte y la hiperemia severa en los numerosos capilares subepidermicos asociados especialmente a areas de necrosis de la epidermis, que se encontraban ocluidos por globulos rojos lisados (nucleos desnudos) a pesar de que el resto de la muestra estaba bien preservada. El tejido conjuntivo de la dermis se aprecio severamente infiltrado por exudado serohemorragico pero con moderada cantidad de heterofilos y leucocitos mononucleares. Los resultados no son totalmente concluyentes respecto a que estas lesiones cutaneas pudieran ser originadas por hemoaglutinacion in vivo pero si se logro constatar que el virus de IA altamente patogeno se replica en gran variedad de celulas incluyendo las endoteliales, lo que pudiera explicar el dano vascular, el incremento de permeabilidad vascular, la extravasacion de gran cantidad de exudado serohemorragico con escasa cantidad de leucocitos, la irrigacion tisular deficiente y por ende, la necrosis de epidermis.
Descriptors: chickens, avian influenza virus, lesions, Veracruz, America, birds, domestic animals, Galliformes, influenza virus, livestock, Mexico, North America, orthomyxoviridae, poultry, useful animals, viruses.
Casaubon, M.T., A. Hernandez, J. Gracia, and M.L. Rosales (1996). Estudo morfologico y consideraciones sobre la evolucion de las lesiones cutaneas causadas por 5 aislamientos de virus de influenza aviar (I.A.) en Mexico. [Morphological study and considerations on the evolution of skin lesions caused by 5 avian influenza virus isolates in Mexico]. Proceedings of the Western Poultry Diseases Conference 45: 48-50.
NAL Call Number: SF995.W4
Descriptors: skin, lesions, avian influenza virus, Mexico, America, body parts, influenza virus, integument, Latin America, North America, orthomyxoviridae, viruses.
Chen, H., G. Deng, Z. Li, G. Tian, Y. Li, P. Jiao, L. Zhang, Z. Liu, R.G. Webster, and K. Yu ( 2004). The evolution of H5N1 influenza viruses in ducks in southern China. Proceedings of the National Academy of Sciences of the United States of America 101(28): 10452-7. ISSN: 0027-8424.
NAL Call Number: 500 N21P
Abstract: The pathogenicity of avian H5N1 influenza viruses to mammals has been evolving since the mid-1980s. Here, we demonstrate that H5N1 influenza viruses, isolated from apparently healthy domestic ducks in mainland China from 1999 through 2002, were becoming progressively more pathogenic for mammals, and we present a hypothesis explaining the mechanism of this evolutionary direction. Twenty-one viruses isolated from apparently healthy ducks in southern China from 1999 through 2002 were confirmed to be H5N1 subtype influenza A viruses. These isolates are antigenically similar to A/Goose/Guangdong/1/96 (H5N1) virus, which was the source of the 1997 Hong Kong "bird flu" hemagglutinin gene, and all are highly pathogenic in chickens. The viruses form four pathotypes on the basis of their replication and lethality in mice. There is a clear temporal pattern in the progressively increasing pathogenicity of these isolates in the mammalian model. Five of six H5N1 isolates tested replicated in inoculated ducks and were shed from trachea or cloaca, but none caused disease signs or death. Phylogenetic analysis of the full genome indicated that most of the viruses are reassortants containing the A/Goose/Guangdong/1/96-like hemagglutinin gene and the other genes from unknown Eurasian avian influenza viruses. This study is a characterization of the H5N1 avian influenza viruses recently circulating in ducks in mainland China. Our findings suggest that immediate action is needed to prevent the transmission of highly pathogenic avian influenza viruses from the apparently healthy ducks into chickens or mammalian hosts.
Descriptors: ducks virology, evolution, molecular, influenza A virus, avian genetics, avian pathogenicity, influenza, avian virology, chickens, China, genes, viral genetics, genotype, avian transmission, mice, molecular sequence data, phylogeny, virulence.
Clavijo, A., J. Riva, J. Copps, Y. Robinson, and E.M. Zhou (2001). Assessment of the pathogenicity of an emu-origin influenza A H5 virus in ostriches (Struthio camelus). Avian Pathology 30(1): 83-89. ISSN: 0307-9457.
NAL Call Number: SF995.A1A9
Abstract: Ostriches were inoculated with a laboratory-derived highly pathogenic avian influenza (HPAI) virus of emu origin, A/emu/TX/39924/93 (H5N2) clone c1B. The aim of this study was to evaluate the pathogenicity of this isolate for ostriches and assess the ability of routine virological and serological tests to detect infection. Avian influenza virus (AIV) was isolated from cloacal and tracheal swabs from 2 to 12 days post-infection. AIV was also isolated from brain, thymus, eyelid, spleen, ovary/testis, liver, air sac, proventriculum, duodenum, caecal tonsil, heart, pancreas, kidney, nasal gland and lung. Virus isolation was also possible from swabs of the luminal surfaces of the cloaca, jejunum, lower ileum, bursa of Fabricius, trachea and bone marrow. Birds seroconverted as early as 7 days post-infection. This study suggests that HPAI virus of emu origin replicates extensively in infected ostriches without causing significant clinical disease or mortality.
Descriptors: ostriches, influenza virus A, pathogenicity, viral replication, trachea, cloaca, animal tissues, isolation, seroconversion, clinical aspects.
Clavijo, A., J. Riva, and J. Pasick (2003). Pathogenicity of a ratite-origin influenza A H5 virus in ostriches (Struthio camelus). Avian Diseases 47(Special Issue): 1203-1207. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Ostriches were inoculated with a highly pathogenic avian influenza (HPAI) virus of ratite origin, A/emu/Texas/39924/93 (H5N2) clone c1B. The aim of this study was to evaluate the pathogenicity of this isolate for ostriches and to assess the ability of routine virologic and serologic tests to detect infection. Avian influenza virus (AIV) was isolated from tracheal swabs from 2 to 12 days postinfection and from cloacal swabs from 3 to 10 days postinfection. AIV was also isolated from a wide range of tissues. Birds seroconverted as early as 7 days postinfection. This study indicates that HPAI virus of ratite origin replicates extensively in infected ostriches without causing significant clinical disease or mortality.
Descriptors: infection, virology, influenza, respiratory system disease, viral disease, serology clinical techniques, diagnostic techniques, viral pathogenicity.
Conrad, R.D. (1971). Characterization and pathogenesis in turkeys of an avian influenza A-like virus (Myxovirus meleagrium) (A Turkey/California/1/64). Dissertation Abstracts International, B 31(9): 5445-5446.
NAL Call Number: Z5055.U49D53
Descriptors: influenza, pathogenesis, turkeys, characterization, Myxovirus meleagrium.
Cooley, A.J., H. Van Campen, M.S. Philpott, B.C. Easterday, and V.S. Hinshaw (1989). Pathological lesions in the lungs of ducks infected with influenza A virus. Veterinary Pathology 26(1): 1-5. ISSN: 0300-9858.
NAL Call Number: 41.8 P27
Descriptors: experimental infection, lungs, ducks, Anas platyrhynchos, avian influenza virus.
Cooley, A.J., H. Van Campen, M.S. Philpott, B.C. Easterday, and V.S. Hinshaw (1989). Pathological lesions in the lungs of ducks infected with influenza A viruses. Veterinary Pathology 26(1): 1-5. ISSN: 0300-9858.
NAL Call Number: 41.8 P27
Abstract: To determine histopathological damage in the respiratory tract, ducks were inoculated with five different influenza A viruses, including viruses virulent for other avian hosts. Lungs were collected for detection of virus and histopathological examination. Small amounts of infectious virus were recovered from lungs, and viral antigens were demonstrated by immunoperoxidase staining with monoclonal antibodies to the viral nucleoprotein. Although clinical signs were not detected, lungs of ducks infected with both virulent and avirulent viruses had mild pneumonia characterized by infiltrates of lymphocytes and macrophages. These findings show that although clinical signs are not evident, ducks may have damage to the respiratory tract during influenza.
Descriptors: ducks, fowl plague pathology, lung pathology, immunoenzyme techniques, influenza A virus avian pathogenicity, virulence.
Cunha, R.G., W.S. Passos, and M.C. Souza (1993). Patogenicidade dos virus de Influenza equina para pintos. [Pathogenicity of equine influenza viruses in chickens]. Revista Brasileira De Biologia 53(1): 29-36. ISSN: 0034-7108.
NAL Call Number: 442.8 R326
Abstract: In the present paper the pathogenicity of equine subtype A/equi 1 (H7N7) and A/equi 2 (H3N8) for chicks was studied. Strains previously isolated in Brazil, representatives of both subtypes, were used. Eight experiments were performed for A/equi 2, using 89 chicks (4 to 18-day old). Six hundred thirty three samples of cloacal material were collected from 01 to 15 days pos-infection (p.i.) and inoculated in 11-day old chick embryos for recuperation of virus. Twelve samples showed positive results. The recuperated viruses were identified with specific antiserum in hemagglutination inhibition test (HI). Blood samples of all chicks collected prior to infection showed no antibodies to both subtypes. Chicks inoculated with A/equi 2 virus were bled 18 to 21 days p.i. Out of 89, seventy one (79.8%) serums showed different levels of antibodies at HI tests. Seventy chicks were inoculated with A/equi 1 subtype. Five hundred forty three samples of cloacal material were harvested and inoculated in embryonated chick eggs. No recuperation of virus occurred. However, all the inoculated chickens showed seroconversion. Chicks infected with A/equi 2 may shed virus in feces. No signs of disease were noted in the inoculated chicks.
Descriptors: chickens microbiology, influenza A virus avian pathogenicity, pathogenicity, chick embryo, cloaca microbiology, hemagglutinins viral immunology, avian immunology, immunology, time factors.
Dybing, J.K., S. Schultz Cherry, D.E. Swayne, D.L. Suarez, and M.L. Perdue (2000). Distinct pathogenesis of hong kong-origin H5N1 viruses in mice compared to that of other highly pathogenic H5 avian influenza viruses. Journal of Virology 74(3): 1443-50. ISSN: 0022-538X.
NAL Call Number: QR360.J6
Abstract: In 1997, an outbreak of virulent H5N1 avian influenza virus occurred in poultry in Hong Kong (HK) and was linked to a direct transmission to humans. The factors associated with transmission of avian influenza virus to mammals are not fully understood, and the potential risk of other highly virulent avian influenza A viruses infecting and causing disease in mammals is not known. In this study, two avian and one human HK-origin H5N1 virus along with four additional highly pathogenic H5 avian influenza viruses were analyzed for their pathogenicity in 6- to 8-week-old BALB/c mice. Both the avian and human HK H5 influenza virus isolates caused severe disease in mice, characterized by induced hypothermia, clinical signs, rapid weight loss, and 75 to 100% mortality by 6 to 8 days postinfection. Three of the non-HK-origin isolates caused no detectable clinical signs. One isolate, A/tk/England/91 (H5N1), induced measurable disease, and all but one of the animals recovered. Infections resulted in mild to severe lesions in both the upper and lower respiratory tracts. Most consistently, the viruses caused necrosis in respiratory epithelium of the nasal cavity, trachea, bronchi, and bronchioles with accompanying inflammation. The most severe and widespread lesions were observed in the lungs of HK avian influenza virus-infected mice, while no lesions or only mild lesions were evident with A/ck/Scotland/59 (H5N1) and A/ck/Queretaro/95 (H5N2). The A/ck/Italy/97 (H5N2) and the A/tk/England/91 (H5N1) viruses exhibited intermediate pathogenicity, producing mild to moderate respiratory tract lesions. In addition, infection by the different isolates could be further distinguished by the mouse immune response. The non-HK-origin isolates all induced production of increased levels of active transforming growth factor beta following infection, while the HK-origin isolates did not.
Descriptors: influenza virology, influenza A virus avian pathogenicity, human pathogenicity, hn protein, Hong Kong, immunohistochemistry, influenza pathology, avian isolation and purification, avian physiology, human isolation and purification, human physiology, mice, mice inbred BALB c, respiratory system pathology, respiratory system virology, transforming growth factor beta blood, virulence, virus replication.
El Sayed, A.M.S., M.M.A. Moustafa, A.A. Amin, M.A. El Sisi, A.H.T. Abd El Nasser, and M.S.M. Hamouda. (1998). Isolation, identification and pathogenicity of an avian influenza virus from ducks in Egypt. In: Proceedings of the 5th Scientific Conference of the Egyptian Veterinary Poultry Association, Cairo (Egypt); Cairo Univ. (Egypt), The Egyptian Veterinary Poultry Association: Cairo, Egypt, p. 29-49.
Descriptors: ducks, avian influenza virus, hemagglutination tests, antibodies, isolation techniques, identification, pathogenicity, Egypt, Africa, agglutination tests, Anseriformes, biological properties, birds, domestic animals, immunological factors, immunological techniques, influenza virus, livestock, microbial properties, North Africa, orthomyxoviridae, poultry, useful animals, viruses.
Forman, A.J., I.M. Parsonson, and W.J. Doughty ( 1986). The pathogenicity of an avian influenza virus isolated in Victoria. Australian Veterinary Journal 63(9): 294-6. ISSN: 0005-0423.
NAL Call Number: 41.8 Au72
Abstract: An influenza virus (H7N7) isolated from an outbreak of disease in chickens in Victoria, was examined for its ability to cause disease in inoculated chickens, turkeys and ducks. The virus was highly pathogenic in chickens and turkeys but produced no clinical disease in ducks. Transmission of infection occurred from inoculated chickens to those in direct contact but other chickens separated by a distance of 3m directly downwind developed neither clinical disease nor antibody to the virus.
Descriptors: chickens microbiology, fowl plague microbiology, influenza A virus avian isolation and purification, poultry diseases microbiology, Australia, avian pathogenicity.
Forsyth, W.M., D.C. Grix, and C.A. Gibson (1993). Diagnosis of highly pathogenic avian influenza in chickens: Bendigo 1992. Australian Veterinary Journal 70(3): 118-9. ISSN: 0005-0423.
NAL Call Number: 41.8 Au72
Descriptors: disease outbreaks veterinary, fowl plague epidemiology, influenza A virus avian immunology, antibodies, viral analysis, chickens, Victoria epidemiology.
Ghendon, Y.Z., A.T. Marchenko, S.G. Markushin, D.B. Ghenkina, A.V. Mikhejeva, and E.E. Rozina (1973). Correlation between TS phenotype and pathogenicity of some animal viruses. Archiv Fur Die Gesamte Virusforschung 42(2): 154-9. ISSN: 0003-9012.
NAL Call Number: 448.3 Ar23
Descriptors: influenza A virus avian pathogenicity, mutation, polioviruses pathogenicity, brain microbiology, chick embryo, chickens, cytopathogenic effect, viral, genetic complementation test, haplorhini, HeLa cells, influenza A virus avian growth and development, influenza A virus avian isolation and purification, Macaca, mutagens, phenotype, polioviruses growth and development, polioviruses isolation and purification, spinal cord microbiology, temperature, tissue culture, virus cultivation, virus replication.
Guo Xiaofeng, Liao Ming, and Xin Chaoa (2000). Studies on the pathogenicity of H9n2 subtype influenza virus. [Distribution of avian influenza virus in chickens and chick embryos by histopathology and immunihistochemistry]. Huanan Nongye Daxue Xuebao [Journal of South China Agricultural University] 22(3): 70-2. ISSN: 1001-411X.
Descriptors: avian influenza virus, H9N2 subtype, pathogenicity, biological properties, microbial properties.
Guo, Y.J., S. Krauss, D.A. Senne, I.P. Mo, K.S. Lo, X.P. Xiong, M. Norwood, K.F. Shortridge, R.G. Webster, and Y. Guan (2000). Characterization of the pathogenicity of members of the newly established H9N2 influenza virus lineages in Asia. Virology 267(2): 279-88. ISSN: 0042-6822.
NAL Call Number: 448.8 V81
Abstract: The reported transmission of avian H9N2 influenza viruses to humans and the isolation of these viruses from Hong Kong poultry markets lend urgency to studies of their ecology and pathogenicity. We found that H9N2 viruses from North America differ from those of Asia. The North American viruses, which infect primarily domestic turkeys, replicated poorly in inoculated chickens. Phylogenetic analysis of the hemagglutinin and nucleoprotein genes indicated that the Asian H9N2 influenza viruses could be divided into three sublineages. Initial biological characterization of at least one virus from each lineage was done in animals. Early isolates of one lineage (A/Chicken/Beijing/1/94, H9N2) caused as high as 80% mortality rates in inoculated chickens, whereas all other strains were nonpathogenic. Sequence analysis showed that some isolates, including the pathogenic isolate, had one additional basic amino acid (A-R/K-S-S-R-) at the hemagglutinin cleavage site. Later isolates of the same lineage (A/Chicken/Hong Kong/G9/97, H9N2) that contains the PB1 and PB2 genes similar to Hong Kong/97 H5N1 viruses replicated in chickens, ducks, mice, and pigs but were pathogenic only in mice. A/Quail/Hong Kong/G1/97 (H9N2), from a second lineage that possesses the replicative complex similar to Hong Kong/97 H5N1 virus, replicated in chickens and ducks without producing disease signs, was pathogenic in mice, and spread to the brain without adaptation. Examples of the third Asian H9N2 sublineage (A/Chicken/Korea/323/96, Duck/Hong Kong/Y439/97) replicated in chickens, ducks, and mice without producing disease signs. The available evidence supports the notion of differences in pathogenicity of H9N2 viruses in the different lineages and suggests that viruses possessing genome segments similar to 1997 H5N1-like viruses are potentially pathogenic in mammals. Copyright 2000 Academic Press.
Descriptors: influenza A virus avian genetics, influenza A virus avian pathogenicity, binding sites genetics, chickens virology, DNA complementary chemistry, DNA complementary genetics, glycosylation, hemagglutinins viral genetics, hemagglutinins viral metabolism, Hong Kong epidemiology, mice, mice inbred BALB c virology, molecular sequence data, phylogeny, poultry diseases epidemiology, RNA viral genetics, reverse transcriptase polymerase chain reaction, sequence analysis, DNA, virulence genetics, virus replication.
Hafez, H.M. (2003). Gefluegelpest: Alte Krankheit mit staendiger Gefahr fuer Gefluegel. [Highly pathogenic avian influenza in poultry]. Tierarztliche Umschau 58(7): 343-351. ISSN: 0049-3864.
NAL Call Number: 41.8 T445
Abstract: "Highly pathogenic" avian influenza viruses cause fowl plague. The disease is a notifiable disease. In 2003 infections with highly pathogenic avian influenza were reported in the Netherlands, Belgium and Germany. Influenza viruses seem to be host specific. The risk of infection of humans with avian influenza A viruses is very low, however, in some cases people can attract infections. This observation should be seriously evaluated. The measures adopted to control and eradicate avian influenza are based on the strategy of stamping-out infected flocks and controlling the movement of poultry, poultry products and other contaminated materials. In general vaccinations against HPAI are only allowed as a supplement to the control measures. The decision to introduce the vaccine is accompanied with several restrictions. This paper explores the characteristics of avian influenza viruses, epidemiology, the disease and public health aspects. Finally, the current control strategy in the European communities is discussed.
Descriptors: epidemiology, infection, veterinary medicine, avian influenza, diagnosis, epidemiology, etiology, pathology, respiratory system disease, symptom, therapy, transmission, viral disease, vaccination clinical techniques, differential diagnosis, public health, zoonosis.
Hooper, P.T. (1989). Lesions in chickens experimentally infected with 1985 H7N7 avian influenza virus. Australian Veterinary Journal 66(5): 155-156. ISSN: 0005-0423.
NAL Call Number: 41.8 Au72
Abstract: In groups receiving intranasal inoculations, 22 of 24 birds became affected. Illnesses were usually less than 2 d with clinical signs generally depression and dullness. Examination of lesions showed that this strain of virus produced in the laboratory a consistent, characteristic disease pattern, affecting predominantly the bursa of Fabricius, the pancreas and the brain.
Descriptors: chickens, avian influenza virus, wounds, pathology, birds, domestic animals, domesticated birds, Galliformes, influenza virus, lesions, livestock, poultry, useful animals, viruses.
Jirjis, F.F., S.L. Noll, D.A. Halvorson, K.V. Nagaraja, and D.P. Shaw (2002). Pathogenesis of avian pneumovirus infection in turkeys. Veterinary Pathology 39(3): 300-10. ISSN: 0300-9858.
NAL Call Number: 41.8 P27
Abstract: Avian pneumovirus (APV) is the cause of a respiratory disease of turkeys characterized by coughing, ocular and nasal discharge, and swelling of the infraorbital sinuses. Sixty turkey poults were reared in isolation conditions. At 3 weeks of age, serum samples were collected and determined to be free of antibodies against APV, avian influenza, hemorrhagic enteritis, Newcastle disease, Mycoplasma gallisepticum, Mycoplasma synoviae, Mycoplasma meleagridis, Ornithobacterium rhinotracheale, and Bordetella avium. When the poults were 4 weeks old, they were inoculated with cell culture-propagated APV (APV/Minnesota/turkey/2a/97) via the conjunctival spaces and nostrils. After inoculation, four poults were euthanatized every 2 days for 14 days, and blood, swabs, and tissues were collected. Clinical signs consisting of nasal discharge, swelling of the infraorbital sinuses, and frothy ocular discharge were evident by 2 days postinoculation (PI) and persisted until day 12 PI. Mild inflammation of the mucosa of the nasal turbinates and infraorbital sinuses was present between days 2 and 10 PI. Mild inflammatory changes were seen in tracheas of poults euthanatized between days 4 and 10 PI. Antibody to APV was detected by day 7 PI. The virus was detected in tissue preparations and swabs of nasal turbinates and infraorbital sinuses by reverse transcription polymerase chain reaction, virus isolation, and immunohistochemical staining methods between days 2 and 10 PI. Virus was detected in tracheal tissue and swabs between days 2 and 6 PI using the same methods. In this experiment, turkey poults inoculated with tissue culture-propagated APV developed clinical signs similar to those seen in field cases associated with infection with this virus.
Descriptors: metapneumovirus growth and development, paramyxoviridae infections veterinary, poultry diseases pathology, turkeys, antibodies, viral blood, Cercopithecus aethiops, cytopathogenic effect, viral, DNA, viral chemistry, DNA, viral genetics, enzyme linked immunosorbent assay veterinary, fluorescent antibody technique veterinary, histocytochemistry veterinary, metapneumovirus genetics, Minnesota, nasal mucosa pathology, nasal mucosa virology, paramyxoviridae infections blood, paramyxoviridae infections pathology, paramyxoviridae infections virology, poultry diseases virology, reverse transcriptase polymerase chain reaction veterinary, vero cells.
Jones, Y.L. and D.E. Swayne (2004). Comparative pathobiology of low and high pathogenicity H7N3 Chilean avian influenza viruses in chickens. Avian Diseases 48(1): 119-28. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: 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.
Descriptors: chickens, influenza A virus, avian pathogenicity, avian virology, chick embryo, Chile, avian classification, avian isolation and purification, avian pathology, virulence.
Karunakaran, D., D.A. Halvorson, V. Sivanandan, and J.A. Newman (1988). Pathogenicity of avian influenza viruses isolated from wild mallard ducks and domestic turkeys. Avian Diseases 32(2): 319-23. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Groups of turkeys were exposed to different isolates of avian influenza virus from wild mallard ducks and domestic turkeys by the intracerebral, intravenous, intratracheal, and intra-airsac routes, and pathogenicity indices were calculated. For the intracerebral pathogenicity study, body weight was also measured. For intravenous, intratracheal, and intra-airsac pathogenicity studies, necropsy lesions were scored and serological responses were recorded. Only the intracerebral pathogenicity index and body weight gain post intracerebral infection demonstrated any differences between isolates. The other procedures failed to demonstrate any pathogenicity whatsoever. There was a correlation (R = 0.73) between intracerebral pathogenicity index and reduced weight gain postinfection. These studies suggest that growth suppression may be an objective measure of pathogenic potential of influenza viruses found to be nonpathogenic by other methods.
Descriptors: ducks microbiology, influenza A virus avian pathogenicity, turkeys microbiology, body weight veterinary, ducks growth and development, ducks immunology, fowl plague immunology, fowl plague physiopathology, hemagglutination inhibition tests veterinary, avian immunology, turkeys growth and development, turkeys immunology.
Katz, J.M., X. Lu, A.M. Frace, T. Morken, S.R. Zaki, and T.M. Tumpey (2000). Pathogenesis of and immunity to avian influenza A H5 viruses. Biomedicine and Pharmacotherapy Biomedecine and Pharmacotherapie 54(4): 178-87. ISSN: 0753-3322.
NAL Call Number: R41.B52
Abstract: In 1997 in Hong Kong, 18 human cases of respiratory illness were caused by an avian influenza A H5N1 virus. Although avian influenza viruses had not previously been known to cause respiratory illness in humans, the H5N1 viruses caused severe illness and death, primarily in individuals aged > 12 years. The introduction of H5N1 viruses into humans raised concerns about the potential of these viruses to cause a pandemic. We have used the BALB/c mouse to better understand the pathogenesis of and immunity to the H5N1 viruses in a mammalian model. Previously, we demonstrated that H5N1 viruses isolated from humans replicated efficiently in the lungs of mice without prior adaptation to this host. Two general phenotypes of pathogenicity of H5N1 viruses, based on high and low lethality for mice, were observed. We now demonstrate that in addition to a lethal outcome, H5N1 viruses with a high pathogenicity phenotype exhibit additional features that include rapid and uncontrolled replication in the lungs of infected mice, dissemination and replication of the virus in other organs, and depletion of peripheral blood leukocytes. The BALB/c mouse model was also used to better understand the parameters of protective immunity to the H5N1 viruses. Prior infection with H5N1 viruses of low pathogenicity or an antigenically related non-pathogenic H5N3 virus protected mice from death by infection with a highly pathogenic HK/483 virus. Serum hemagglutination-inhibition antibody titers of 40 or greater were associated with protection of mice from death. Immunization of mice with baculovirus-expressed recombinant H5 hemagglutinin protein or a previously defined HS-specific synthetic peptide induced MHC class II restricted CTL activity. Mice that had CTL activity but no serum hemagglutination-inhibition antibody were not protected from a lethal challenge with H5N1 virus. These results suggest that antibody is required for protection of mice against lethal challenge with H5N1 viruses of the high pathogenicity phenotype.
Descriptors: influenza A virus avian immunology, avian pathogenicity, antibodies, viral blood, antigens, viral analysis, immunization, influenza virology, influenza vaccine immunology, mice, mice inbred BALB c, T lymphocytes, cytotoxic immunology, virus replication.
Kawaoka, Y. (1991). Difference in replication and pathogenicity of influenza A viruses in chickens and mice. Journal of Veterinary Medical Science the Japanese Society of Veterinary Science 53(1): 125-6. ISSN: 0916-7250.
NAL Call Number: SF604.J342
Descriptors: chickens microbiology, influenza A virus avian physiology, porcine physiology, influenza A virus physiology, mice microbiology, cloaca microbiology, avian pathogenicity, porcine pathogenicity, influenza A virus pathogenicity, orthomyxoviridae infections microbiology, orthomyxoviridae infections veterinary, poultry diseases microbiology, rodent diseases microbiology, trachea microbiology, virus replication.
Kobayashi, Y., T. Horimoto, Y. Kawaoka, D. Alexander, and C. Itakura (1996). Pathological studies of chickens experimentally infected with two highly pathogenic avian influenza viruses. Avian Pathology 25(2): 285-304. ISSN: 0307-9457.
NAL Call Number: SF995.A1A9
Abstract: Lesions of chickens inoculated with two highly pathogenic avian influenza virus strains, A/turkey/England/50-92/91 (H5N1) and A/chicken/Victoria/1/85 (H7N7) were examined histologically and immunohistochemically. Birds of both treatment groups died within 5 days post-inoculation. The most significant lesions induced by these two viruses consisted of swelling of the microvascular endothelium, systemic congestion, multifocal haemorrhages, perivascular mononuclear cell infiltration, and thrombosis associated with viral antigen in the vascular endothelium and/or perivascular parenchymatous cells. Viral antigen in the cardiac myocytes was consistently detected in all birds. In addition, severe pulmonary congestion and oedema was found in A/turkey/England/50-92/91 virus-inoculated birds that died within 1 day post-inoculation. The other chickens of both groups showed necrotic and inflammatory changes associated with viral antigen in various organs and tissues. These findings suggested that cardiovascular system involvement played an important role in the pathogenesis of these virus infections.
Descriptors: animal husbandry, immune system, infection, methods and techniques, morphology, pathology, veterinary medicine, avian influenza virus, avian pathology, experimental infections, histological, immunohistochemical examination, infection lesions, necrotic, inflammatory changes, pathological studies, pathology, viral antigen, viral infection pathogenesis.
Kobayashi, Y., T. Horimoto, Y. Kawaoka, D.J. Alexander, and C. Itakura (1996). Neuropathological studies of chickens infected with highly pathogenic avian influenza viruses. Journal of Comparative Pathology 114(2): 131-147. ISSN: 0021-9975.
NAL Call Number: 41.8 J82
Abstract: Central nervous system lesions of chickens inoculated with three highly pathogenic avian influenza virus strains, A/chicken/Victoria/ 1/85 (H7N7), A/turkey/England/50-92/91 (H5N1), and A/tern/South Africa/61 (H5N3), were examined histologically and immunohistochemically. The chickens either died within 7 days of inoculation or were killed 2 weeks after inoculation. No significant differences were observed in the lesions induced by these three viruses. The lesions were divided into two types, disseminated foci of microgliosis and necrosis, and ventriculitis. The former lesions were associated with infection of the vascular endothelium and dissemination of the virus to the peripheral parenchymal cells of the chickens that died within 3 days of inoculation. The ventriculitis lesions, however, were observed mainly in the chickens that died between 4 and 7 days after inoculation. These findings suggest that viral infection of the vascular endothelium and subsequent involvement of ependymal cells play important roles in the pathogenesis of the central nervous system lesions.
Descriptors: animal husbandry, cell biology, infection, morphology, nervous system, pathology, veterinary medicine, central nervous system, lesion, comparative pathology, ependymal cell microgliosis, necrosis, pathogenesis, photomicrograph, vascular endothelium, ventriculitis.
Lalithakunjamma, C.R. and M. Mini (1991). Pathology of the chick embryo infected with avian influenza virus. Journal of Veterinary and Animal Sciences 22(2): 94-98. ISSN: 0971-0701.
NAL Call Number: SF604.K42
Abstract: The sequential pathologic changes in the chick embryo infected with influenza virus were described. Degenerative and necrotic changes were seen in most of the organs. Oedema was very prominent. Heterophilic involvement was not a characteristic feature of the embryo response to Avian influenza virus.
Descriptors: animal husbandry, development, infection, veterinary medicine.
Laudert, E.A. (1993). Pathogenesis of Avian Influenza Virus Infection in Mallard Ducks, p. vi, 131 leaves, ill.
Descriptors: avian influenza, mallard ducks, pathogenesis, infection.
Li YanBing, Tian GuoBin, Tian KeGong, Chen HuaLan, and Yu KangZhen (2004). Identification of H7N2 avian influenza virus and pathogenicity analysis in chicken and mice. Animal Biotechnology Bulletin 9(1): 391-396. ISSN: 1014-8469.
Descriptors: antibody formation, diagnostic techniques, experimental infection, hemagglutination inhibition test, immune response, pathogenicity, strain differences, virulence, avian influenza virus, chickens, mice.
Lomniczi, B. (2004). Avian influenza and Newcastle disease: pathogenicity, epidemiology and evolution - comments on the definition of the diseases [A madarinfluenza es a baromfipestis (Newcastle-betegseg): patogenitas, epidemiologia es evolucio - megjegyzesek a betegsegek definiciojahoz]. Magyar Allatorvosok Lapja 126(2): 87-100. ISSN: 0025-004X.
NAL Call Number: 41.8 V644
Descriptors: disease prevalence, epidemiology, evolution, pathogenicity, Newcastle disease, avian influenza virus.
Luo KaiJian, Liang ZhaoPing, Zhao MingQiu, Liao Ming, Guo XiaoFeng, Ren Tao, Zhang GuiHong, Cao WeiSheng, and Xin ChaoAn (2004). Studies on the immunogenicity of avian influenza virus strain A/Chicken/Guangdong/SS/94 (H9N2) by paraffin section. Chinese Journal of Zoonoses 20(3): 196-198, 202. ISSN: 1002-2694.
Descriptors: avian influenza virus, histopathology, immunization, inactivated vaccines, fowl.
Manvell, R.J., C. English, P.H. Jorgensen, and I.H. Brown (2003). Pathogenesis of H7 influenza A viruses isolated from ostriches in the homologous host infected experimentally. Avian Diseases 47(Special Issue): 1150-1153. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: 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.
Descriptors: infection, veterinary medicine, avian influenza, infectious disease, respiratory system disease, viral disease, disease pathogenesis, immune response, virus excretion, ostrich.
Mo, I.P., M. Brugh, O.J. Fletcher, G.N. Rowland, and D.E. Swayne (1997). Comparative pathology of chickens experimentally inoculated with avian influenza viruses of low and high pathogenicity. Avian Diseases 41(1): 125-136. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Pathologic changes and distribution of viral antigen as determined by immunohistochemistry were compared among 4-wk-old specific-pathogen-free chickens inoculated intratracheally with avian influenza virus (AIV) isolates of either low or high pathogenicity. Viruses of low pathogenicity previously characterized as mildly pathogenic (MP), included A/chicken/Pennsylvania/21525/83 (H5N2) (MP-Penn) and A/chicken/Alabama/7395/75 (H4N8) (MP-Alab). Viruses of high pathogenicity included A/chicken/Pennsylvania/1370/83 (H5N2), A/chicken/Victoria/A185/85 (H7N7), and A/turkey/Ontario/7732/66 (H5N9). Extremely variable clinical signs ranging from mild respiratory distress to high mortality were present among chickens inoculated with these viruses. Chickens inoculated with highly pathogenic (HP) virus had histologic lesions of necrosis and inflammation in cloacal bursa, thymus, spleen, heart, pancreas, kidney, brain, trachea, lung, and skeletal muscle, whereas chickens inoculated with HP virus had histologic lesions most frequently in lung and trachea or lacked histologic lesions. Immunospecific staining for avian influenza viral proteins was most common in cells within heart, lung, kidney, brain, and pancreas of chickens inoculated with HP viruses, but immunospecific staining was present only and infrequently in trachea and lung of chickens inoculated with MP-Penn AIV. MP-Alab did not produce lesions nor have vital antigen in inoculated chickens but did produce serologic evidence of infection. The pattern of organ involvement and viral antigen distribution in chickens intratracheally inoculated with HP MV isolates indicates a common capability to spread beyond the respiratory tract and confirms the pantrophic replicative, pathobiologic, and lethal nature of the viruses. However, variability in severity and lesion distribution exists between different HP AIVs.
Descriptors: chickens, avian influenza virus, pathogenicity, experimental infection, in vivo experimentation, histopathology, lesions, antigens, animal tissues, biological properties, birds, body parts, disease transmission, domestic animals, domesticated birds, experimentation, Galliformes, immunological factors, infection, influenza virus, livestock, microbial properties, orthomyxoviridae, pathogenesis, pathology, poultry, useful animals, viruses, viral antigens.
Mutinelli, F., I. Capua, C. Terregino, and G. Ortali (2001). Clinical, gross and microscopic findings in different Avian species naturally infected by type A, highly pathogenic Avian influenza virus of the H7N1 subtype. Proceedings of the Western Poultry Diseases Conference 50: 12-15.
NAL Call Number: SF995.W4
Descriptors: avian influenza virus, pathogenicity, pathotypes, birds.
Mutinelli, F., H. Hablovarid, and I. Capua (2003). Avian embryo susceptibility to Italian H7N1 avian influenza viruses belonging to different lineages. Avian Diseases 47(Special Issue): 1145-1149. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: An immunohistochemical investigation was performed to assess tissue tropism and viral replication of Italian H7N1 isolates belonging to different lineages in developing chicken, turkey, Muscovy duck, and mallard duck embryos. Low-pathogenic avian influenza (LPAI) isolates were selected on the basis of the location in the phylogenetic tree; a progenitor strain, A/turkey/Italy/977/V99 (exhibiting no additional glycosylation sites, nAGS), strain A/turkey/Italy/2379/V99 (AGS in position 123), and strain A/turkey/Italy/3675/V99 (AGS in position 149) were selected. The latter two strains belonged to distinct lineages originating from the pool of progenitor strains. The highly pathogenic avian influenza (HPAI) isolate A/turkey/Italy/4580/V99 was also included in the test. All the embryos tested supported the growth of HPAI. The LPAI isolates replicated readily in the allantoic layer of the chorioallantoic membrane of all the species tested and did not replicate to detectable levels in the developing chicken, turkey, and Muscovy duck embryos. In contrast, they replicated to different extents in the respiratory tract of the developing mallard embryo. The findings indicate that the pathogenesis of LPAI infections in mallard embryos is different to that observed in other species and should be investigated further.
Descriptors: development, infection, avian influenza, infectious disease, respiratory system disease, viral disease, immunohistochemistry immunologic techniques, laboratory techniques, avian embryo infection susceptibility pathogenesis viral replication.
Ogawa, T., T. Sugimura, S. Itohara, Y. Tanaka, and T. Kumagai (1980). Intracerebral pathogenicity of influenza A viruses for chickens. Archives of Virology 64(4): 383-6. ISSN: 0304-8608.
NAL Call Number: 448.3 Ar23
Abstract: The virulence of influenza A viruses was determined using the intracerebral pathogenicity index test for chickens. The viruses were divided into high virulent, low virulent and avirulent strains. A low virulent strain was recovered from the jejunum and faeces of infected chickens.
Descriptors: brain microbiology, chickens microbiology, influenza A virus pathogenicity, feces microbiology, influenza A virus avian pathogenicity, influenza A virus human pathogenicity, influenza A virus, porcine pathogenicity, influenza A virus growth and development, jejunum microbiology.
Otsuki, K., Y. Kawaoka, T. Nakamura, and M. Tsubokura (1982). Pathogenicity for chickens of avian influenza viruses isolated from whistling swans and a black-tailed gull in Japan. Avian Diseases 26(2): 314-20. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: We isolated 24 Hav1 Neq1 and 18 Hav6 Nav3 influenza viruses from such free-living wild waterfowl as whistling swans, black-tailed gulls, and tufted ducks in western Japan in 1980. Two Hav1 Neq1 viruses isolated from a whistling swan and a black-tailed gull and a Hav6 Nav3 virus from a whistling swan were examined for their pathogenicity for chickens. Five-week-old specific-pathogen-free chickens were inoculated with the viruses intratracheally or intraperitoneally. Virus was recovered successfully from all the organs, including the brain, despite the absence of signs of disease. The intracerebral pathogenicity index scores obtained for the Hav1 Neq1 viruses were 0.43 and 0.87; the score for the Hav6 Nav3 virus was 0.43. No virus produced plaques in cultivated chick embryo fibroblast cells in the absence of trypsin.
Descriptors: animal population groups microbiology, animals, wild microbiology, birds microbiology, chickens microbiology, ducks microbiology, influenza A virus avian pathogenicity, chick embryo, Japan, specific pathogen free organisms, terminology.
Otsuki, K., K. Yamazaki, Y. Kawaoka, and M. Tsubokura (1988). Intracerebral pathogenicity for chickens of avian influenza viruses isolated from free-living waterfowl in Japan. Veterinary Microbiology 18(3-4): 357-62. ISSN: 0378-1135.
NAL Call Number: SF601.V44
Abstract: The pathogenicity for chickens of 91 strains of avian influenza A virus isolated from such free-living waterfowl as whistling swan, pintail, tufted duck, mallard and black-tailed gull in Japan was tested. The majority of the virus strains infected and were pathogenic for the chickens. The virulence of these viruses seemed not to be as high as that of fowl plague virus. There were no significant differences in the intracerebral index score among the viruses belonging to the same subtype, irrespective of year of isolation or host.
Descriptors: birds microbiology, brain diseases veterinary, chickens microbiology, fowl plague microbiology, influenza A virus avian pathogenicity, brain diseases microbiology, fowl plague transmission, influenza A virus avian isolation and purification, seasons, virulence.
Padilla, N.R., F.E. Aburto, C.M. Fraire, and N.L. Padilla (2004). Influenza aviar: histopatologia y deteccion viral por rt-pcr en tejidos fijados con formalina e incluidos en parafina. [Avian influenza: histopathology and viral detection in formalin-fixed, paraffin-embedded tissues by RT-PCR]. Veterinaria Mexico 35(1): 1-19. ISSN: 0301-5092.
NAL Call Number: SF604.V485
Descriptors: infection, acute renal tubular necrosis, avian influenza, non suppurative encephalitis, vasculitis, reverse transcription polymerase chain reaction, clinical techniques, diagnostic techniques, viral replication, chickens.
Perdue, M.L. (2000). How can a virus suddenly become very pathogenic? World Poultry (Special): 9-10. ISSN: 1388-3119.
NAL Call Number: SF481.M54
Descriptors: avian influenza virus, highly pathogenic, mutations, poultry.
Perkins, L.E. and D.E. Swayne (2001). Pathobiology of A/chicken/Hong Kong/220/97 (H5N1) avian influenza virus in seven gallinaceous species. Veterinary Pathology 38(2): 149-64. ISSN: 0300-9858.
NAL Call Number: 41.8 P27
Abstract: 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.
Descriptors: birds virology, fowl plague pathology, influenza A virus avian pathogenicity, poultry diseases virology, adrenal glands pathology, antigens, viral blood, brain pathology, chick embryo, fowl plague virology, hemorrhage veterinary, immunohistochemistry veterinary, lung pathology, poultry diseases pathology, pulmonary edema veterinary, specific pathogen free organisms, splenomegaly veterinary.
Perkins, L.E.L. and D.E. Swayne (2003). Varied pathogenicity of a Hong Kong-origin H5N1 avian influenza virus in four Passerine species and budgerigars. Veterinary Pathology 40(1): 14-24. ISSN: 0300-9858.
NAL Call Number: 41.8 P27
Descriptors: avian influenza virus, experimental infections, lesions, pathogenicity, species differences, wild birds, budgerigars, Passer domesticus, Carpodacus mexicanus, Sternus vulgaris, Taeniopygia guttata.
Perkins, L.E.L. and D.E. Swayne (2002). Pathogenicity of a Hong Kong-origin H5N1 highly pathogenic avian influenza virus for emus, geese, ducks, and pigeons. Avian Diseases 46(1): 53-63. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: The H5N1 type A influenza viruses that emerged in Hong Kong in 1997 are a unique lineage of type A influenza viruses with the capacity to transmit directly from chickens to humans and produce significant disease and mortality in-both of these hosts. The objective of this study was to ascertain the susceptibility of emus (Dramaius novaehollandiae), domestic geese (Anser anser domesticus), domestic ducks (Anas platyrhynchos), and pigeons (Columba livia) to intranasal (i.n.) inoculation with the A/chicken/Hong Kong/220/97 (H5N1) highly pathogenic avian influenza virus. No mortality occurred within 10 days postinoculation (DPI) in the four species investigated, and clinical disease, evident as neurologic dysfunction, was observed exclusively in emus and geese. Grossly, pancreatic mottling and splenomegaly were identified in these two species. In addition, the geese had cerebral malacia and thymic and bursal atrophy. Histologically, both the emus and geese developed pancreatitis, meningoencephalitis, and mild myocarditis. Influenza viral antigen was demonstrated in areas with histologic lesions up to 10 DPI in the geese. Virus was reisolated from oropharyngeal and cloacal swabs and from the lung, brain, and kidney of the emus and geese. Moderate splenomegaly was observed grossly in the ducks. Viral infection of the ducks was pneumotropic, as evidenced by mild inflammatory lesions in the respiratory tract and virus reisolation from oropharyngeal swabs and from a lung. Pigeons were resistant to HK/220 infection, lacking gross and histologic lesions, viral antigen, and reisolation of virus. These results imply that emus and geese are susceptible to i.n. inoculation with the HK/220 virus, whereas ducks and pigeons are more resistant. These latter two species probably played a minimal epidemiologic role in the perpetuation of the H5N1 Hong Kong-origin influenza viruses.
Descriptors: infection, veterinary medicine, H5N1 avian influenza virus infection, etiology, mortality, viral disease, bursal atrophy, joint disease, cerebral malacia, nervous system disease, meningoencephalitis, nervous system disease, myocarditis, heart disease, neurologic dysfunction, nervous system disease, pancreatic mottling, digestive system disease, endocrine disease, pancreas, pancreatitis, digestive system disease, respiratory tract inflammation, respiratory system disease, splenomegaly, blood and lymphatic disease, thymic atrophy, endocrine disease, thymus.
Pysina, T.V. and A.S. Gorbunova (1970). Sootnosheniia mezhdu patogennost'iu virusov grippa ptits dlia laboratornykh zhivotnykh i infitsirovaniem avifauny. [Relation between the pathogenicity of avian influenza viruses for laboratory animals and infection of avifauna]. Voprosy Virusologii 15(3): 298-301. ISSN: 0507-4088.
NAL Call Number: 448.8 P942
Descriptors: bird diseases microbiology, orthomyxoviridae pathogenicity, bird diseases epidemiology, chickens, Czechoslovakia, ducks, England, influenza epidemiology, influenza microbiology, mice, Scotland, Siberia, South Africa, tissue culture, virus cultivation.
Ranck, F.M.J., L.C. Grumbles, C.F. Hall, and J.E. Grimes (1970). Serology and gross lesions of turkeys inoculated with an avian influenza A virus, a paramyxovirus, and Mycoplasma gallisepticum. Avian Diseases 14(1): 54-65. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Descriptors: Mycoplasma infections pathology, orthomyxoviridae infections pathology, poultry diseases, antibody formation, hemagglutination inhibition tests, immune sera analysis, lung diseases pathology, lung diseases veterinary, mycoplasma pathogenicity, Mycoplasma infections immunology, orthomyxoviridae pathogenicity, orthomyxoviridae infections immunology, pulmonary alveoli immunology, pulmonary alveoli microbiology, pulmonary alveoli pathology, turkeys.
Reinacher, M., J. Bonin, O. Narayan, and C. Scholtissek (1983). Pathogenesis of neurovirulent influenza A virus infection in mice. Route of entry of virus into brain determines infection of different populations of cells. Laboratory Investigation a Journal of Technical Methods and Pathology 49(6): 686-92. ISSN: 0023-6837.
NAL Call Number: 448.8 L11
Abstract: Coinfection of a cell culture with a human and avian influenza A virus had yielded a recombinant virus with high neurovirulence for mice. This study reports on the comparative pathogenesis of central nervous system infection in mice between the parental human and the recombinant virus using the immunohistologic peroxidase-antiperoxidase method and virus assay of tissue suspensions. The human virus replicated poorly in mice and did not replicate in the brain even after intracerebral inoculation. In contrast, the recombinant virus replicated to high titer in the lung and brain with resulting viremia after inoculation of young mice by the intracerebral, intraperitoneal, or intranasal routes. Different populations of cells in the brain became infected after inoculation by each of the three routes: choroid plexus, and ependymal and subependymal cells after intracerebral inoculation; cells in perivenous areas, neurons in the olfactory bulbs and trigeminal ganglia and nuclear groups in the brainstem and midbrain after intranasal inoculation. Intraperitoneal inoculation resulted almost exclusively in the perivenous spread of the virus. The intranasal inoculation suggested that virus entry into the brain both by spread along nerve cell processes from the nasal mucosa to the brain and trigeminal ganglia and subsequent perivenous spread after viremia developed following virus replication in the lung. To dissect these two mechanisms we inoculated neonatal mice that had acquired high levels of serum antibody by nursing from actively immunized mothers. Intraperitoneal inoculation of these mice failed to cause infection, whereas intranasal inoculation resulted in the same pattern of cellular spread through the olfactory and trigeminal pathways as noted previously. This proved that this recombinant influenza virus could invade the central nervous system after infection via a natural route of infection. This highly neuroinvasive agent provides one example of the extent of virulence which can be acquired by recombination of apathogenic influenza viruses and raises a note of caution for adequate control of those agents generated in the laboratory.
Descriptors: brain diseases microbiology, influenza microbiology, influenza A virus avian pathogenicity, influenza A virus human pathogenicity, antigens, viral analysis, birds, brain microbiology, brain pathology, brain diseases immunology, brain diseases pathology, immunization, influenza immunology, influenza pathology, influenza A virus avian genetics, influenza A virus avian immunology, influenza A virus human genetics, influenza A virus human immunology, lung microbiology, lung pathology, mice, plaque assay, recombination, genetic, virulence, virus replication.
Resende, M. (1981). Comparative pathogenesis of virulent and avirulent avian influenza viruses in turkeys. Dissertation Abstracts International, B 41(10): 3706.
NAL Call Number: Z5055.U49D53
Descriptors: avian influenza virus, turkeys, pathogenesis.
Rimmelzwaan, G.F., T. Kuiken, A.G. van, T.M. Bestebroer, R.A.M. Fouchier, and A.D.M.E. Osterhaus (2003). A primate model to study the pathogenesis of influenza A (H5N1) virus infection. Avian Diseases 47(Special Issue): 931-933. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Cynomolgus macaques (Macaca fascicularis) infected with influenza virus A/HongKong/156/97 (H5N1) developed acute respiratory distress syndrome (ARDS) with fever. Reverse transcriptase/polymerase chain reaction (RT/PCR) and virus isolation showed that the respiratory tract is the major target of the virus. The main lesion observed upon necropsy, performed 4 or 7 days postinfection, was a necrotizing bronchointerstitial pneumonia, similar to that found in primary influenza pneumonia in human beings. By immunohistochemistry, influenza virus antigen proved to be limited to pulmonary tissue and tonsils. The data indicate that ARDS and multiple organ dysfunction syndrome (MODS), observed in both humans and monkeys infected with this virus, are caused by diffuse alveolar damage from virus replication in the lungs alone.
Descriptors: infection, acute respiratory distress syndrome (ARDS), respiratory system disease, avian influenza, infectious disease, respiratory system disease, viral disease, bronchointerstitial pneumonia, respiratory system disease, multiple organ dysfunction syndrome (MODS), disease miscellaneous, immunohistochemistry immunologic techniques, laboratory techniques, necropsy clinical techniques, reverse transcriptase polymerase chain reaction (RT PCR) genetic techniques, laboratory techniques, viral isolation laboratory techniques, influenza pathogenesis viral replication.
Rott, R. (1982). Determinants of influenza virus pathogenicity. Lecture held on the occasion of the reception of the reception of the Otto-Warburg-Medaille on September 27, 1982. Hoppe Seyler's Zeitschrift Fur Physiologische Chemie 363(11): 1273-82. ISSN: 0018-4888.
NAL Call Number: 384 Z38
Descriptors: orthomyxoviridae pathogenicity, amino acid sequence, cell transformation, viral, hemagglutinins, influenza A virus avian genetics, avian pathogenicity, orthomyxoviridae genetics, plaque assay, RNA viral genetics, species specificity, viral proteins genetics.
Rott, R. (1985). In vitro Differenzierung von pathogenen und apathogenen aviaren Influenzaviren. [In vitro differentiation of pathogenic and nonpathogenic avian influenza viruses]. Berliner Und Munchener Tierarztliche Wochenschrift 98(2): 37-9. ISSN: 0005-9366.
NAL Call Number: 41.8 B45
Descriptors: influenza A virus avian classification, microbiological techniques veterinary, chick embryo, fibroblasts, hemagglutination tests, avian pathogenicity, plaque assay veterinary, tissue culture, virulence, virus cultivation.
Rott, R. (1981). The role of the hemagglutinin in infectivity and pathogenicity of avian influenza viruses. In: Proceedings of the First International Symposium on Avian Influenza, Beltsville, Maryland, USA, p. 116-133.
NAL Call Number: aSF995.6.I6I5 1981a
Descriptors: avian influenza viruses, pathogenicity, infectivity, hemagglutinins, symposium.
Rott, R., H.D. Klenk, Y. Nagai, and M. Tashiro (1995). Influenza viruses, cell enzymes, and pathogenicity. American Journal of Respiratory and Critical Care Medicine 152(4, Pt. 2): S16-9. ISSN: 1073-449X.
Abstract: Proteolytic cleavage of the influenza virus hemagglutinin glycoprotein (HA) by cellular proteases is a prerequisite for virus infectivity, spread of the virus in the infected organism, tissue tropism, and viral pathogenicity. Production of infectious virus depends upon the structure at the HA cleavage site as well as the substrate specificity and the distribution of appropriate enzymes. Differences exist in the specificities of the endoproteases that recognize the different sequence motifs at the cleavage site. With avian influenza viruses that cause lethal systemic infections, the cleavage site consists of multibasic amino acids. Furin, which activates this type of HA, is a member of the subtilisin family and represents the prototype of ubiquitously occurring membrane-bound proteases. On the other hand, serine proteases secreted from a restricted number of cell types and some bacterial enzymes recognize a monobasic cleavage signal at HA of the mammalian and the apathogenic avian influenza viruses. The limited occurrence of these proteases results in only localized infection. Implementation of these defined conditions for virus activation may represent a novel type of disease control.
Descriptors: hemagglutinins viral physiology, orthomyxoviridae enzymology, orthomyxoviridae pathogenicity, serine endopeptidases physiology, subtilisins physiology, furin, hemagglutinins viral chemistry, substrate specificity.
Rott, R., H.D. Klenk, and C. Scholtissek (1984). Bedeutung des Hamagglutinins fur die Pathogenitat aviarer Influenzaviren. [Significance of hemagglutinins for the pathogenicity of avian influenza viruses]. Zentralblatt Fur Bakteriologie, Mikrobiologie, Und Hygiene. Series A, Medical Microbiology, Infectious Diseases, Virology, Parasitology 258(2-3): 337-49. ISSN: 0176-6724.
NAL Call Number: 448.3 C33 (1)
Abstract: In addition to acute viral diseases, persistent infections have attained considerable interest in recent years. Such persistent infections are characterized by extended time periods in which the infecting virus remains within the organism before the eventual appearance of manifest symptoms. These infections may be evoked by a variety of virus species resulting in a diversity of pathogenic reactions and clinical manifestations. The mechanisms of viral persistence, where known, also appear to be quite diverse. As far as space permits, some examples of persistent infections will be presented and the mechanisms of the pathogenesis of the resulting diseases will be discussed.
Descriptors: hemagglutinins viral analysis, hemagglutinins viral genetics, hemagglutinins viral immunology, influenza A virus avian pathogenicity, amino acid sequence, cell membrane microbiology, chick embryo, fetal membranes microbiology, genes viral, avian genetics, avian growth and development, avian ultrastructure, models, molecular, mutation, virulence.
Rott, R., H.D. Klenk, C. Scholtissek, A Kohn (ed.), and P Fuchs (ed.). (1984). On the pathogenicity of avian influenza viruses. In: Mechanisms of viral pathogenesis: from gene to pathogen - Proceedings of the 28th OHOLO Conference, p. 246-256.
NAL Call Number: QP356.3.O4 1983
Descriptors: avian influenza viruses, pathogenicity.
Rott, R., M. Orlich, and C. Scholtissek (1979). Correlation of pathogenicity and gene constellation of influenza A viruses. III. Non-pathogenic recombinants derived from highly pathogenic parent strains. Journal of General Virology 44(2): 471-7. ISSN: 0022-1317.
NAL Call Number: QR360.A1J6
Abstract: We have demonstrated by recombination of two highly pathogenic avian influenza viruses [A/FPV/Rostock (Hav1N1) x A/turkey/England/63 (Hav1Nav3)] that recombinants can be isolated which are pathogenic as well as non-pathogenic for chickens. They carried the glycoproteins of either parent strains, and all are produced in infectious form in chick embryo cells. Genetic analysis revealed that the non-pathogenic recombinants possess a mixed RNA polymerase complex, consisting of pol 1, pol 2, ptra and NP gene products, while, with one exception, the pathogenic recombinants have the genes coding for the polymerase activity from one or other parent virus. The biological properties of the recombinant viruses did not correlate with their pathogenicity for chickens.
Descriptors: genes viral, influenza A virus avian genetics, recombination, genetic, chickens, DNA directed RNA polymerases genetics, fowl plague microbiology, avian pathogenicity, neuraminidase genetics, turkeys.
Samadieh, B. (1975). Cytopathogenic effect of avian influenza-A viruses upon different cell lines. In: 20th World Veterinary Congress. Summaries, Volume 2, p. 1059-1060.
Descriptors: avian influenza A viruses, cytopathogenicity, cell lines.
Scholtissek, C. and R. Rott (1984). Correlation between loss of the temperature-sensitive phenotype and pathogenicity of fowl plague virus mutants in the chicken. Virus Research 1(2): 117-31. ISSN: 0168-1702.
NAL Call Number: QR375.V6
Abstract: The reversion of temperature-sensitive (ts) mutants of fowl plague virus to the ts+ phenotype was correlated with pathogenicity for chicken. Two types of ts mutants were investigated: those obtained by mutagenesis with 5-fluorouracil and those obtained by undiluted passages at 33 degrees C. The reversion frequency of the former mutants depended on the RNA segment in which the ts defect was located, mutations in RNA segments 1 and 2 having the highest reversion frequency, those in the RNA segments coding for the glycoproteins the lowest. ts mutants obtained by undiluted passages behaved differently in this respect. There was an approximate correlation between frequency of reversion and pathogenicity for chicken. Double mutants induced by 5-fluorouracil, having one tight and one leaky mutation, reverted easily without loss of the leaky mutation. These double mutants were still to a limited extent pathogenic for the chicken. Only one double mutant with two tight mutations (ts 293) was completely nonpathogenic after intramuscular inoculation. Two ts mutants with multiple tight defects (ts 1/1 and ts 3/18) obtained by undiluted passage did not revert to wild-type after injection into embryonated eggs and incubation at 33 degrees C, but they were still slightly pathogenic for the chicken. There was no obvious correlation between the shut-off temperature and pathogenicity of mutants carrying a single ts defect. However, for mutants with multiple tight mutations a high shut-off temperature seemed to be essential for reversion during serial passages as well as for pathogenicity in the chicken, when different routes of inoculation were examined. ts mutants seem to be safe as live vaccines only, (1) if they carry at least two tight ts defects, (2) if they have a relatively low shut-off temperature, and (3) if they could be administered other than via the respiratory tract.
Descriptors: influenza A virus avian genetics, mutation, temperature, chickens microbiology, fluorouracil pharmacology, avian pathogenicity.
Scholtissek, C., A. Vallbracht, B. Flehmig, and R. Rott (1979). Correlation of pathogenicity and gene constellation of influenza A viruses. II. Highly neurovirulent recombinants derived from non-neurovirulent or weakly neurovirulent parent virus strains. Virology 95(2): 492-500. ISSN: 0042-6822.
NAL Call Number: 448.8 V81
Descriptors: genes viral, influenza A virus pathogenicity, recombination, genetic, brain microbiology, chickens, influenza A virus avian genetics, human genetics, influenza A virus genetics, lung microbiology, mice, tissue culture, virulence.
Selleck, P.W., G. Arzey, P.D. Kirkland, R.L. Reece, A.R. Gould, P.W. Daniels, and H.A. Westbury (2003). An outbreak of highly pathogenic avian influenza in Australia in 1997 caused by an H7N4 virus. Avian Diseases 47(Special Issue): 806-811. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: In November of 1997 an outbreak of highly pathogenic avian influenza occurred near the town of Tamworth, in northern New South Wales, Australia. The viruses isolated from chickens on two commercial chicken farms were identified as H7N4 viruses, with hemagglutinin cleavage site amino acid sequences of RKRKRG and intravenous pathogenicity indices of 2.52 and 2.90, respectively. A virus with an identical nucleotide sequence, but with an intravenous pathogenicity index of 1.30, was also isolated from cloacal swabs collected from asymptomatic emus kept on a third property.
Descriptors: animal husbandry, epidemiology, infection, avian influenza, infectious disease, respiratory system disease, viral disease, commercial chicken farms, disease outbreaks.
Shalaby, A.A., R.D. Slemons, and D.E. Swayne (1994). Pathological studies of A/chicken/Alabama/7395/75 (H4N8) influenza virus in specific-pathogen-free laying hens. Avian Diseases 38(1): 22-32. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: 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.
Descriptors: fowl plague pathology, influenza A virus avian isolation and purification, chickens, kidney microbiology, kidney pathology, lung microbiology, lung pathology, ovary microbiology, ovary pathology, oviducts microbiology, oviducts pathology, oviposition, specific pathogen free organisms.
Shinya, K., T. Awakura, A. Shimada, F.D. Silvano, T. Umemura, and K. Otsuki (1995). Pathogenesis of pancreatic atrophy by avian influenza A virus infection. Avian Pathology 24(4): 623-632. ISSN: 0307-9457.
NAL Call Number: SF995.A1A9
Abstract: Specific-pathogen-free (SPF), 2-day-old chicks were inoculated with type A influenza virus (A/whistling swan/Shimane/499/83/(H5N3)) into their caudal thoracic air sac. The original isolate of the virus was of low virulence (ICPI 0.20 to 0.40), and was passaged 10 times through the respiratory organs of SPF chicks. Most of the chicks inoculated with the passaged virus (strain 499) showed respiratory and alimentary signs. Three of 30 chicks died on days 2, 6 and 7 post-inoculation (p.i.). Almost half of the infected chicks showed poor growth, and the variation of body size in the flock became prominent from day 10 p.i. Infected chicks consistently had pathological changes in the pancreas, liver, kidneys and respiratory tracts, and occasionally in the brain, duodenum and bone marrow. Positive immunoreaction to avian influenza virus (AIV) antigen and recovery of the virus persisted for longer period in the pancreas than in other organs. The pancreatic lesions were caused by a direct, lytic virus infection of the acinar cells and contributed to poor growth of the chicks.
Descriptors: chicks, avian influenza virus, pancreas, atrophy, pathogenesis, virulence, symptoms, histopathology, growth retardation, acinar cells.
Silvano, F.D., M. Yoshikawa, A. Shimada, K. Otsuki, and T. Umemura (1997). Enhanced neuropathogenicity of avian influenza A virus by passages through air sac and brain of chicks. Journal of Veterinary Medical Science the Japanese Society of Veterinary Science 59(3): 143-8. ISSN: 0916-7250.
NAL Call Number: SF604.J342
Abstract: Three-day-old, specific-pathogen-free (SPF) chicks were inoculated with the strains of influenza A/whistling swan/Shimane/ 499/83 (H5N3) via the air sac route. The strains had been passaged through air sacs or air sacs and brains of SPF chicks. Two experiments were undertaken to examine the pathogenicity of these strains and the development of brain lesions based on time-interval changes. In experiment 1, original strain (4e) showed low pathogenicity with mild respiratory signs and zero mortality. Air sac passaged strains (18a and 24a) of 4e demonstrated mortalities of 50% and 67%, respectively, and inoculated chicks showed hemorrhages and necrotic lesions in major organs. Air sac-brain passaged strain (24a5b) of 4e produced 100% mortality and severe nervous signs. Severe circulatory disturbance with multiple foci of necrosis in major organs including the brain was found in chicks inoculated with 24a5b. The 24a5b was analogous to highly pathogenic avian influenza virus in regard to its pathogenicity to chicks. Hence, low pathogenic influenza virus (4e) gradually aggravated its pathogenicity to highly pathogenic virus (24a5b) by air sac and brain passages. In experiment 2, chicks were inoculated with 24a5b, and the earliest histological lesion was the enlargement of the vascular endothelial cells at 18 hr post-inoculation (PI) followed by necrotizing encephalitis at 24 to 48 hr PI. Immunohistological staining revealed avian influenza virus antigen initially in the vascular endothelial cells and then in the astrocytes, neurons and ependyma.
Descriptors: air sacs virology, brain virology, chickens, fowl plague pathology, influenza A virus pathogenicity, air sacs pathology, antigens, viral analysis, brain immunology, brain pathology, endothelium, vascular pathology, influenza A virus immunology, microscopy, electron methods, microscopy, electron veterinary, necrosis, neurons ultrastructure, serial passage, specific pathogen free organisms, time factors.
Slemons, R.D., P.K. Condobery, and D.E. Swayne ( 1991). Assessing pathogenicity potentical of waterfowl-origin type A influenza viruses in chickens. Avian Diseases 35(1): 210-215. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Intravenous pathogenicity index (IVPI) tests on 29 wild duck-origin type A influenza viruses, two turkey-origin type A influenza viruses, and one chicken-origin type A influenza virus resulted in indices ranging from 0.0 to 0.49. Most of the wild duck-origin viruses and the two turkey-origin viruses had indices of 0.0, indicating they are not pathogenic. Six of the duck-origin viruses had indices ranging from 0.25 to 0.49, and the IVPI for A/chicken/Alabama/75 (H4N8) was 0.49, indicating they had low pathogenic potential. An IVPI of 1.25 up to the maximum score of 3.0 is necessary for a type A influenza virus to be classified as highly pathogenic. Gross lesions observed in chickens dying following intravenous viral challenge included kidney swelling with more prominent lobular patterns, but visceral urate deposits were not present. The usefulness of the IVPI test in evaluating the pathogenicity potential of nonpathogenic and low-pathogenic strains of avian influenza virus may be limited.
Descriptors: fowls, avian influenza virus, waterfowl, ducks, pathogenicity, kidneys, lesions, mortality, Ohio.
Slemons, R.D., L.N. Locke, M.G. Sheerar, R.M. Duncan, V.S. Hinshaw, and B.C. Easterday (1990). Kidney lesions associated with mortality in chickens inoculated with waterfowl influenza viruses. Avian Diseases 34(1): 120-8. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Seventy-six type A influenza viruses recovered from waterfowl in Wisconsin, California, South Dakota, Florida, Texas, Alabama, and Nebraska were tested for virulence in chickens. The challenge to chickens was intravenous inoculation of first-, second-, or third-egg-passage virus. Each of the virus strains was tested separately in three or four chickens. Eighteen of the 76 viruses caused the death of one or more chickens following inoculation. Postmortem lesions were similar in all dead birds. In decreasing order of frequency, gross lesions included: swollen kidneys evident as accentuated lobular patterns, urates in the pericardial sac, and urates on the surface of the liver. Microscopic lesions present in kidneys were consistent with visceral gout. Mortality was associated with inoculations having higher concentrations of infectious virus. These results indicate that the influenza A viruses circulating in duck populations may include strains potentially pathogenic for chickens.
Descriptors: chickens, fowl plague pathology, influenza A virus avian pathogenicity, kidney pathology, animals, wild, antibodies, viral biosynthesis, birds, ducks, fowl plague microbiology, fowl plague mortality, geese, avian immunology, avian isolation and purification, virulence.
Smolenskii, V.I. (1976). Izuchenie patogeneza estestvennogo grippa kur. [Pathogenesis of spontaneous influenza of fowls]. Sbornik Nauchnykh Trudov, Moskovskaya Veterinarnaya Akademiya 87: 73-77.
Descriptors: avian influenza virus, immunofluorescence technique, pathogenesis.
Swayne, D.E. (1997). Pathobiology of H5N2 Mexican avian influenza virus infections of chickens. Veterinary Pathology 34(6): 557-67. ISSN: 0300-9858.
NAL Call Number: 41.8 P27
Abstract: To determine the association between specific structural changes in the hemagglutinin gene and pathogenicity of avian influenza viruses (AIVs), groups of 4-week-old White Plymouth Rock chickens were inoculated intravenously or intranasally with AIVs of varying pathogenicities isolated from chickens in central Mexico during 1994-1995. Mildly pathogenic (MP) viruses had a common hemagglutinin-connecting peptide sequence of Pro-Gln-Arg-Glu-Thr-Arg decreases Gly and had restricted capability for replication and production of lesions in tissues. The principle targets for virus replication or lesion production were the lungs, lymphoid organs, and visceral organs containing epithelial cells, such as kidney and pancreas. Death was associated with respiratory and/or renal failure. By contrast, highly pathogenic (HP) AIVs had one substitution and the addition of two basic amino acids in the hemagglutinin connecting peptide, for a sequence of Pro-Gln-Arg-Lys-Arg-Lys-Thr-Arg decreases Gly. The HP AIVs were pantropic in virus replication and lesion production ability. However, the most severe histologic lesions were produced in the brain, heart, adrenal glands, and pancreas, and failure of multiple critical organs was responsible for disease pathogenesis and death. No differences in lesion distribution patterns or in sites of AIV replication were evident to explain the variation in mortality rates for different HP AIVs, but HP AIVs that produced the highest mortality rates had more severe necrosis in heart and pancreas. The ability of individual HP AIVs to produce low or high mortality rates could not be explained by changes in sequence of the hemagglutinin-connecting peptide alone, but probably required the addition of other undetermined genomic changes.
Descriptors: chickens, fowl plague pathology, influenza A virus avian genetics, avian pathogenicity, avian physiology, adrenal glands chemistry, adrenal glands pathology, adrenal glands virology, brain pathology, brain virology, brain chemistry, fowl plague epidemiology, fowl plague mortality, hemagglutinins viral chemistry, hemagglutinins viral genetics, immunohistochemistry, kidney chemistry, kidney pathology, kidney virology, Mexico epidemiology, myocardium chemistry, myocardium pathology, pancreas chemistry, pancreas pathology, pancreas virology, specific pathogen free organisms, spleen chemistry, spleen pathology, spleen virology, viral proteins analysis, viral proteins metabolism, virus replication.
Swayne, D.E., M.L. Perdue, M. Garcia, E. Rivera Cruz, and M. Brugh (1997). Pathogenicity and diagnosis of H5N2 Mexican avian influenza viruses in chickens. Avian Diseases 41(2): 335-346. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Chickens were inoculated with one of five H5N2 Mexican-origin avian influenza virus (AIV) isolates to determine their pathogenicity for chickens and to determine the ability of routine virologic and serologic tests to detect infections. In laboratory infections, three AIVs, H5/94, M5/94, and J12/94, produced sporadic illness and death and were categorized as mildly pathogenic. Q1/95 produced illness and death in all inoculated chickens and was categorized as highly lethal and highly pathogenic (HP). P11/94B commonly produced clinical illness, but deaths were infrequent. During the presence of clinical signs, oropharyngeal swabs were superior for isolation of AIV; but cloacal swabs were more successful after disappearance of clinical signs. Agar gel precipitin (AGP) serologic test was superior for detecting AIV infection during the clinical phase, but AGP and hemagglutinin inhibition tests were equally effective in detecting infections after recovery from clinical illness. Passage of P11/94B parent stock and selected 14-day-embryo-passed AIVs in adult hens resulted in emergence of some HP AIV derivatives. The hemagglutinin of Q1/95 and P11/94B parent stock and derivative AIVs had an identical proteolytic cleavage site of....Pro- Gln-Arg-Lys-Arg-Lys-Thr-Arg decreased Gly, consistent with AIVs of high pathogenicity. However, no consistent differences were identified in the sequence of the hemagglutinin gene to explain the discrepancy in lethality patterns of the P11/94B AIVs. This suggests that genes other than the hemagglutinin impact the full expression of high lethality of Mexican-origin AIV infections in chickens.
Descriptors: Mexico, chickens, avian influenza virus, pathogenicity, diagnosis, immunodiffusion tests, hemagglutination tests, chemical composition, agglutination tests, America, biological properties, birds, domestic animals, domesticated birds, Galliformes, immunological techniques, immunoprecipitation tests, influenza virus, Latin America, livestock, microbial properties, North America, orthomyxoviridae, poultry, useful animals, viruses, oropharyngeal swabs, cloacal swabs, molecular sequence data, hemagglutination inhibition test, amino acid sequences.
Swayne, D.E. and R.D. Slemons (1994). Comparative pathology of a chicken-origin and two duck-origin influenza virus isolates in chickens: the effect of route of inoculation. Veterinary Pathology 31(2): 237-45. ISSN: 0300-9858.
NAL Call Number: 41.8 P27
Abstract: Forty-nine 5-week-old chickens were inoculated by the intravenous (i.v.), intratracheal (IT), or intranasal (IN) routes with either a chicken-origin or one of two duck-origin type A influenza virus isolates. Twelve control chickens were inoculated with sterile chorioallantoic fluid. For all viruses, i.v. inoculation produced predominate lesions of renal tubule necrosis (nephrosis) and nephritis, and influenza virus nucleoprotein was localized in nuclei and cytoplasm of necrotic renal tubule epithelium. Chickens inoculated by the IT route, and to a lesser extent the IN route, had mild to severe tracheitis, bronchitis, and ventromedial pneumonia associated with secondary bronchi but lacked renal tubule necrosis and nephritis. These data indicate low-virulence avian-origin influenza viruses were nephrotropic during simulated systemic infection (i.v. inoculation) and pneumotropic during simulated local infection (IT and IN inoculation). Gross and histologic kidney lesions produced by i.v. inoculation of the chicken-origin influenza virus were similar to changes reported in outbreaks of low-virulence influenza virus in laying chickens.
Descriptors: chickens microbiology, ducks microbiology, fowl plague pathology, influenza A virus avian pathogenicity, poultry diseases pathology, acute disease, administration, intranasal, immunohistochemistry, injections, intravenous, intubation, intratracheal, virulence.
Swayne, D.E. and R.D. Slemons (1995). Comparative pathology of intravenously inoculated wild duck- and turkey-origin type A influenza viruses in chickens. Avian Diseases 39(1): 74-84. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: Five-week-old specific-pathogen-free chickens were inoculated intravenously with one of 16 low-pathogenicity type A influenza virus isolates; 14 were of wild duck origin, and two were of turkey origin. Tubulointerstitial nephritis was the most frequent specific histopathologic change. The frequency and severity of kidney lesions were independent of the virus hemagglutinin-neuraminidase subtype or titer of the challenge virus. Influenza nucleoprotein was most frequently demonstrated in the kidney and was consistently localized to necrotic proximal and/or distal renal tubule epithelium. Common nonspecific histopathologic changes were lymphoid hyperplasia of the spleen and cecal tonsils, as well as lymphocyte depletion in the cloacal bursa. Uncommon histopathologic changes, in decreasing order of frequency, were interstitial pneumonia, lymphoid follicular hyperplasia in the myocardium, and lymphocytic tracheitis. Histopathologic changes were rare or absent in the jejunum, duodenum, pancreas, and brain. The low-pathogenicity avian-origin type A influenza virus isolates were epitheliotropic in chickens, primarily nephrotropic. Such findings were dissimilar from findings with highly pathogenic avian-origin type A influenza virus isolates both in severity and in tissue distribution of histopathologic changes and influenza viral antigen.
Descriptors: fowl plague pathology, influenza A virus avian pathogenicity, antigens, viral analysis, chickens, ducks, immunohistochemistry, avian isolation and purification, nephritis pathology, nephritis virology, organ specificity, species specificity, turkeys.
Tashiro, M., M. Reinacher, and R. Rott (1987). Aggravation of pathogenicity of an avian influenza virus by adaptation to quails. Archives of Virology 93(1-2): 81-95. ISSN: 0304-8608.
NAL Call Number: 448.3 Ar23
Abstract: Influenza virus A/turkey/Ontario/7732/66 (H 5 N 9), which is highly pathogenic to chickens, is nonpathogenic to quails. After intratracheal or intramuscular inoculation of quails, virus replication was limited to the respiratory tract, genital organs, and pancreas. However, aggravation of the pathogenicity was achieved through adaptation only by several passages of lung homogenates in quails. The adapted virus caused a fatal generalized infection in quails as well as in chickens. The pathogenic change of the virus could not be explained by a change in the proteolytic cleavability of the hemagglutinin, because no difference was found in the cleavability between the original and the adapted viruses. The adapted virus formed larger plaques and grew a little faster than the original one in both chicken embryo and quail embryo cells. The faster multiplication of the adapted virus at the site of infection might be the reason for its change in pathogenicity. The original virus could circulate among quails by a direct contact transmission without causing disease. The shed virus, however, caused a fatal infection in chickens when they were kept in contact with the infected quails. The epidemiological significance of this observation is discussed.
Descriptors: Coturnix microbiology, fowl plague microbiology, influenza A virus avian pathogenicity, quail microbiology, adaptation, physiological, antibodies, viral analysis, antigens, viral analysis, central nervous system microbiology, chickens microbiology, hemagglutinins viral analysis, avian immunology, ribonucleoproteins analysis, turkeys microbiology, virus replication.
To, K.F., P.K. Chan, K.F. Chan, W.K. Lee, W.Y. Lam, K.F. Wong, N.L. Tang, D.N. Tsang, R.Y. Sung, T.A. Buckley, J.S. Tam, and A.F. Cheng (2001). Pathology of fatal human infection associated with avian influenza A H5N1 virus. Journal of Medical Virology 63(3): 242-6 . ISSN: 0146-6615.
Abstract: Eighteen cases of human influenza A H5N1 infection were identified in Hong Kong from May to December 1997. Two of the six fatal cases had undergone a full post-mortem which showed reactive hemophagocytic syndrome as the most prominent feature. Other findings included organizing diffuse alveolar damage with interstitial fibrosis, extensive hepatic central lobular necrosis, acute renal tubular necrosis and lymphoid depletion. Elevation of soluble interleukin-2 receptor, interleukin-6 and interferon-gamma was demonstrated in both patients, whereas secondary bacterial pneumonia was not observed. Virus detection using isolation, reverse transcription-polymerase chain reaction and immunostaining were all negative. It is postulated that in fatal human infections with this avian subtype, initial virus replication in the respiratory tract triggers hypercytokinemia complicated by the reactive hemophagocytic syndrome. These findings suggest that the pathogenesis of influenza A H5N1 infection might be different from that of the usual human subtypes H1-H3.
Descriptors: influenza pathology, influenza virology, influenza A virus avian isolation and purification, adolescent, adult, bone marrow pathology, cytokines blood, disease outbreaks, fatal outcome, Hong Kong epidemiology, influenza epidemiology, lung pathology, lymphoid tissue pathology, postmortem changes.
Tumpey, T.M., D.L. Suarez, L.E.L. Perkins, D.A. Senne, J. Lee, Y.J. Lee, I.P. Mo, H.W. Sung, and D.E. Swayne (2003 ). Evaluation of a high-pathogenicity H5N1 avian influenza A virus isolated from duck meat. Avian Diseases 47(Special Issue): 951-955. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: The introduction of an influenza A virus possessing a novel hemagglutinin (HA) into an immunologically naive human population has the potential to cause severe disease and death. Such was the case in 1997 in Hong Kong, where H5N1 influenza was transmitted to humans from infected poultry. Because H5N1 viruses are still isolated from domestic poultry in southern China, there needs to be continued surveillance of poultry and characterization of virus subtypes and variants. This study provides molecular characterization and evaluation of pathogenesis of a recent H5N1 virus isolated from duck meat that had been imported to South Korea from China. The HA gene of A/Duck/Anyang/AVL-1/01 (H5N1) isolate was found to be closely related to the Hong Kong/97 H5N1 viruses. This virus also contained multiple basic amino acids adjacent to the cleavage site between HA1 and HA2, characteristic of high-pathogenicity avian influenza viruses (HPAI). The pathogenesis of this virus was characterized in chickens, ducks, and mice. The DK/Anyang/AVL-1/01 isolate replicated well in all species and resulted in 100% and 22% lethality for chickens and mice, respectively. No clinical signs of disease were observed in DK/Anyang/AVL-1/01-inoculated ducks, but high titers of infectious virus could be detected in multiple tissues and oropharyngeal swabs. The presence of an H5N1 influenza virus in ducks bearing a HA gene that is highly similar to those of the pathogenic 1997 human/poultry H5N1 viruses raises the possibility of reintroduction of HPAI to chickens and humans.
Descriptors: epidemiology, infection, duck meat, contamination, poultry product, immunologically naive populations, pathogenesis, viral introduction, viral transmission.
United States. Animal and Plant Health Inspection Service. (2001). Highly Pathogenic Avian Influenza: a Threat to U.S. Poultry, Program Aid, Vol. 1704, United States. Dept. of Agriculture: [Washington, DC]: The Service, 1 folded sheet 8 p.
NAL Call Number: 1 Ag84Pro no. 1704
Descriptors: nonindigenous pests control, United States, avian influenza, threat, poultry.
van der Goot, J.A., G. Koch, M.C.M. de Jong, and M. Van Boven (2003). Transmission dynamics of low- and high-pathogenicity A/Chicken/Pennsylvania/83 avian influenza viruses. Avian Diseases 47(Special Issue): 939-941. ISSN: 0005-2086.
NAL Call Number: 41.8 Av5
Abstract: High-pathogenicity avian influenza (HPAI) viruses emerged from low-pathogenicity avian influenza (LPAI) viruses in Pennsylvania (1983-84), Mexico (1994-95), and Italy (1999-2000). Here we focus on the question of why the HPAI virus supersedes the LPAI virus, once it has appeared during the epidemic. To study this, we used an experimental model in chickens that enabled us to estimate the reproduction ratio (R0). Using this model, we determined the R0 of the A/Chicken/Pennsylvania/21525/83 (LPAI) and of the A/Chicken/Pennsylvania/1370/83 (HPAI). Comparing the R0 of both viruses, we concluded that the R0 of the HPAI virus is significantly higher than the R0 of the LPAI.
Descriptors: epidemiology, infection, avian influenza, infectious disease, respiratory system disease, viral disease, transmission dynamics.
Vertinskii, K.I. and A.P. Strel' nikov (1974). Gripp kur. [Avian influenza: pathological studies]. Sbornik Nauchnykh Trudov Moskovskaya Veterinarnaya Akademiya 73(Pt. 1): 122-125.
Descriptors: pathology, fowl, lesions, symptoms, Moscow region, avian influenza.
Yamagiwa, A. and C. Itakura (1970). [Fowl plague prevailing in Manchuria. 4. Central nervous system lesions in chickens inoculated experimentally with fowl plague virus through serial passage]. Nippon Juigaku Zasshi Japanese Journal of Veterinary Science 32(5): 251-6. ISSN: 0021-5295.
NAL Call Number: 41.8 J27
Descriptors: central nervous system pathology, fowl plague pathology, chickens, China, influenza A virus avian, virus cultivation.
Zambon, M.C. (1999). Epidemiology and pathogenesis of influenza. Journal of Antimicrobial Chemotherapy 44(Suppl. B): 3-9. ISSN: 0305-7453.
NAL Call Number: RM260.J6
Abstract: Influenza A, B and C all have a segmented genome, although only certain influenza A subtypes and influenza B cause severe disease in humans. The two major proteins of influenza are the surface glycoproteins-haemagglutinin (HA) and neuraminidase (NA). HA is the major antigen for neutralizing antibodies and is involved in the binding of virus particles to receptors on host cells. Pandemics are a result of novel virus subtypes of influenza A, created by reassortment of the segmented genome (antigenic shift), whereas annual epidemics are a result of evolution of the surface antigens of influenza A and B virus (antigenic drift). The rapid evolution of influenza viruses highlights the importance of surveillance in identifying novel circulating strains. Infectivity of influenza depends on the cleavage of HA by specific host proteases, whereas NA is involved in the release of progeny virions from the cell surface and prevents clumping of newly formed virus. In birds, the natural hosts of influenza, the virus causes gastrointestinal infection and is transmitted via the faeco-oral route. Virulent avian influenza strains, which cause systemic disease, have an HA that is cleaved by proteases present in all cells of the body, rather than by proteases restricted to the intestinal tract. In mammals, replication of influenza subtypes appears restricted to respiratory epithelial cells. Most symptoms and complications, therefore, involve the respiratory tract. However, systemic complications are sometimes observed and other viral genes besides the HA, including the NA, may be involved in determination of virulence of influenza strains in mammals.
Descriptors: antigenic variation physiology, hemagglutinin glycoproteins, influenza virus physiology, influenza epidemiology, neuraminidase physiology, antiviral agents therapeutic use, influenza drug therapy, influenza virology, influenza A virus human pathogenicity, neuraminidase antagonists and inhibitors, sialic acids therapeutic use.
Zambon, M.C. (2001). The pathogenesis of influenza in humans. Reviews in Medical Virology 11(4): 227-41. ISSN: 1052-9276.
Descriptors: antigenic variation physiology, influenza virology, orthomyxoviridae pathogenicity, orthomyxoviridae physiology, antigenic variation genetics, birds virology, disease reservoirs, evolution, molecular, hemagglutinin glycoproteins, influenza virus chemistry, hemagglutinin glycoproteins, influenza virus genetics, hemagglutinin glycoproteins, influenza virus metabolism, influenza epidemiology, influenza transmission, neuraminidase genetics, neuraminidase metabolism, orthomyxoviridae enzymology, orthomyxoviridae genetics.
Zitzow, L.A., T. Rowe, T. Morken, W.J. Shieh, S. Zaki, and J.M. Katz (2002). Pathogenesis of avian influenza A (H5N1) viruses in ferrets. Journal of Virology 76(9): 4420-9. ISSN: 0022-538X.
NAL Call Number: QR360.J6
Abstract: Highly pathogenic avian influenza A H5N1 viruses caused outbreaks of disease in domestic poultry and humans in Hong Kong in 1997. Direct transmission of the H5N1 viruses from birds to humans resulted in 18 documented cases of respiratory illness, including six deaths. Here we evaluated two of the avian H5N1 viruses isolated from humans for their ability to replicate and cause disease in outbred ferrets. A/Hong Kong/483/97 virus was isolated from a fatal case and was highly pathogenic in the BALB/c mouse model, whereas A/Hong Kong/486/97 virus was isolated from a case with mild illness and exhibited a low-pathogenicity phenotype in mice. Ferrets infected intranasally with 10(7) 50% egg infectious doses (EID(50)) of either H5N1 virus exhibited severe lethargy, fever, weight loss, transient lymphopenia, and replication in the upper and lower respiratory tract, as well as multiple systemic organs, including the brain. Gastrointestinal symptoms were seen in some animals. In contrast, weight loss and severe lethargy were not noted in ferrets infected with 10(7) EID(50) of two recent human H3N2 viruses, although these viruses were also isolated from the brains, but not other extrapulmonary organs, of infected animals. The results demonstrate that both H5N1 viruses were highly virulent in the outbred ferret model, unlike the differential pathogenicity documented in inbred BALB/c mice. We propose the ferret as an alternative model system for the study of these highly pathogenic avian viruses.
Descriptors: disease models, animal, ferrets, influenza physiopathology, influenza A virus avian pathogenicity, adolescent, child, preschool, influenza pathology, influenza virology, lung pathology, lung virology, virulence, virus replication.