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,