Dtsch Tierarztl Wochenschr. 2004 Dec; 111(12): 467-72
Review of the literature on avian influenza A viruses in
pigeons and
experimental studies on the susceptibility of domestic
pigeons to influenza
A viruses of the haemagglutinin subtype H7.
Kaleta EF, Honicke A.
Klinik fur Vogel, Reptilien, Amphibien und Fische,
Fachbereich Veterinarmedizin, Justus-
Liebig-Universitat Giessen, Frankfurter.
erhard.f.kaleta@vetmed.uni-giessen.de
The scientific literature of the past century is reviewed on
fowl plague (presently termed
highly pathogenic avian influenza, HPAI) in pigeons. HPAI
viruses cause epidemic
disease outbreaks with high rates of losses in many avian
species, particularily in
chickens and turkeys. Also susceptible to disease are
quails, guinea fowl, ducks, geese,
ostriches, passerine birds, and birds of prey whereas
conflicting reports on the
susceptibility of the domestic pigeon exist. Based on
literature reports and on own
experiments, and applying as criteria for judgements
clinically overt forms of disease,
virus multiplication plus shedding and seroconversion, it is
concluded that domestic
pigeons are only partially susceptible to influenza A
viruses of the haemagglutinin subtype
H7. Infection of pigeons with H7 viruses results only in
some of them in signs, virus
shedding and seroconversion. Using the same criteria,
pigeons appear to be even less
susceptible to infection with influenza A viruses of the H5
subtype. Only one of five
publications describe in 1/19 pigeons exposed to H5
influenza A virus depression one day
before death, and only 2/19 multiplied and excreted virus,
and 1/19 developed circulating
antibodies. Consequently, pigeons play only a minor role in
the epidemiology of H5
influenza viruses. In contrast, following infection with
influenza A virus of the subtype H7
clinical signs in pigeons consist of conjunctivitis, tremor,
paresis of wings and legs, and
wet droppings. H7-infected pigeons multiply and excrete H7
viruses and develop
circulating antibodies. Albeit of the status of infection,
free-flying domestic pigeons can
act as mechanical vectors and vehicles for long-distance
transmission of any influenza A
virus if plumage or feet were contaminated.
Avian Pathol. 2004 Oct 33 (5): 492-505
Investigation of outbreaks of highly pathogenic H5N1 avian
influenza in
waterfowl and wild birds in Hong Kong in late 2002.
Ellis TM, Bousfield RB, Bissett LA, Dyrting KC, Luk GS, Tsim
ST, Sturm-Ramirez K,
Webster RG, Guan Y, Malik Peiris JS.
Tai Lung Veterinary Laboratory, Agriculture Fisheries and
Conservation Department, Lin
Tong Mei, Sheung Shui, New Territories, Hong Kong SAR,
China. ellis_trevor@afcd.gov.hk
Outbreaks of highly pathogenic H5N1 avian influenza have
occurred in Hong Kong in
chickens and other gallinaceous poultry in 1997, 2001, twice
in 2002 and 2003. High
mortality rates were seen in gallinaceous birds but not in
domestic or wild waterfowl or other
wild birds until late 2002 when highly pathogenic H5N1 avian
influenza occurred in
waterfowl (geese, ducks and swans), captive Greater Flamingo
(Phoenicopterus ruber) and
other wild birds (Little Egret Egretta garzetta) at two
waterfowl parks and from two dead
wild Grey Heron (Ardea cinerea) and a Black-headed Gull (Larus
ridibundus) in Hong Kong.
H5N1 avian influenza virus was also isolated from a dead
feral pigeon (Columba livia) and a
dead tree sparrow (Passer montanus) during the second
outbreak. The first waterfowl
outbreak was controlled by immediate strict quarantine and
depopulation 1 week before the
second outbreak commenced. Control measures implemented for
the second outbreak
included strict isolation, culling, increased sanitation and
vaccination. Outbreaks in
gallinaceous birds occurred in some live poultry markets
concurrently with the second
waterfowl outbreak, and infection on a chicken farm was
detected 1 week after the second
waterfowl park outbreak was detected, on the same day the
second grey heron case was
detected. Subsequent virus surveillance showed the outbreaks
had been contained.
The susceptibility of pigeons to Avian Influenza
A/chicken/Germany/2003
(H7N7)
O. Werner , E. Starick and J.P. Teifke
Bundesforschungsanstalt für Viruskrankheiten der Tiere Insel
Riems, Germany
11 pigeons were inoculated oculonasal with the HPAIV subtype
H7N7. 1 pigeon wasn’t
infected and was the control. On day 1 post-infection, they
placed in the same room 6 young
SPF-chickens, who stayed together with the pigeons whole the
time.4 SPF-chickens were
inoculated oculonasal with the same virus in another room.
On day 1 - 6 –8 –10 –14 post-
infection, they took a throat and cloaca swab for virus
isolation. On day 3 and 6 post
infection, they did euthanasia on 2 pigeons and 10 different
organs were taken for virus-
isolation and anatomo-pathological research. Bloodsamples
were taken on the day before
infection, and on day 14 – 23 – 28 – 36 post-infection,
searching for antibodies against Avian
Influenza subtype 7. They did euthanasia after 36 days on
all animals followed by an
anatomo-pathological research and took bloodsamples. 2 from
the 4 SPF-chickens that were
infected got diarrhea, on day 2 they all were ill, on day 3
+ 4 they all died.
The infected pigeons stayed all healthy without any
symptoms, just like the non-infected
pigeon. There were even no clinical signs and anatomo-pathological
they couldn’t see any
sign. The SPF-chickens who were in the same room and were
not experimental inoculated
showed also no clinical and anatomo-pathological sign at
all. Virus isolation out of the inner
organs were all negative. They could do a virusisolation out
of the throat swabs from 9 of the
11 pigeons on day 1, and 2 from 11 out of the cloaca swab.
On day 2 this was respectively 4
and 4. On day 3, 3 pigeons and on day 4 and 5 they could
isolate virus out of the throat
swabs, but from day 6 on everything was negative. Apparently
there is a very small
multiplication of the virus, and also some shedding of the
virus, but not enough for infecting
the SPF-chickens. In one pigeon stayed everything negative,
just as the control animal during
the time of research. The antibody titer was in 5 from 7
(who lived during the whole research
period) low and never higher than 24, except from 2 animals.
This can be seen as a reaction
against the inoculum, because the control animal was always
negative. There were never
antibodies in the SPF-chickens that weren’t infected.
Important note: The pigeons will never be infected with such
a high dose of virus as in this
research was done.
Avian Dis. 2003; 47 (3 Suppl) 849-56
The quest of influenza A viruses for new hosts.
Liu M, Guan Y,Peiris M, He S, Webby RJ, Perez D, Webster RG.
St. Jude Children's Research Hospital, Division of Virology,
Department of Infectious
Diseases, 332 N. Lauderdale, Memphis, TN 38105, USA.
There is increasing evidence that stable lineages of
influenza viruses are being
established in chickens. H9N2 viruses are established in
chickens in Eurasia, and there
are increasing reports of H3N2, H6N1, and H6N2 influenza
viruses in chickens both in
Asia and North America. Surveillance in a live poultry
market in Nanchang, South
Central China, reveals that influenza viruses were isolated
form 1% of fecal samples
taken from healthy poultry over the course of 16 months. The
highest isolation rates were
from chickens (1.3%) and ducks (1.2%), followed by quail
(0.8%), then pigeon (0.5%).
H3N6, H9N2, H2N9, and H4N6 viruses were isolated from
multiple samples, while single
isolates of H1N1, H3N2, and H3N3 viruses were made.
Representatives of each virus
subtype were experimentally inoculated into both quail and
chickens. All the viruses
replicated in the trachea of quail, but efficient
replication in chickens was confined to
25% of the tested isolates. In quail, these viruses were
shed primarily by the aerosol
route, raising the possibility that quail may be the "route
modulator" that changes the
route of transmission of influenza viruses from fecal-oral
to aerosol transmission. Thus,
quail may play an important role in the natural history of
influenza viruses. The pros and
cons of the use of inactivated and recombinant fowl
pox-influenza vaccines to control the
spread of avian influenza are also evaluated.
Avian Dis. 2002 Jan-Mar; 46(1): 53-63.
Pathogenicity of a Hong Kong-origin H5N1 highly pathogenic
avian
influenza virus for emus, geese, ducks, and pigeons.
Perkins LE, Swayne DE.
Southeast Poultry Research Laboratory, United States
Department of Agriculture,
Agricultural Research Service, Athens, GA 30605, USA.
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.
Avian Dis. 1996 Jul-Sep; 40 (3): 600-4
Susceptibility of pigeons to avian influenza.
Panigrahy B, Senne DA, Pedersen JC, Shafer AL, Pearson JE.
National Veterinary Services Laboratories, U.S. Department
of Agriculture, Ames, Iowa
50010, USA.
Susceptibility to infection with avian influenza virus (AIV)
was studied in pigeons inoculated
via oculonasal (Experiment 1) or intravenous (Experiment 2)
route. Chickens were included
as susceptible hosts in both experiments. Two subtypes each
of the highly pathogenic AIV
(HPAIV; HP CK/PA H5N2 and HP CK/Australia H7N7) and
non-pathogenic AIV (NPAIV;
NP CK/PA H5N2 and NP emu/TX H7N1) at a dose of 10(5) embryo
infective dose per bird
were used as inoculum. The pigeons inoculated with HP CK/PA
H5N2 or HP CK/Australia
H7N7 remained apparently healthy throughout the 21-day
observation period, did not shed
viruses on 3, 7, 14, and 21 days postinoculation (DPI), and
had no demonstrable levels of
antibodies on 21 DPI. On the other hand, 9 of 12 chickens
inoculated with the HPAIV died of
highly pathogenic avian influenza; the viruses were
recovered from their respiratory and
intestinal tissues, and the surviving chickens had
antibodies to AIV. Regarding responses of
pigeons to inoculation with NP CK/PA H5N2 or NP emu/TX H7N1,
the pigeons remained
clinically healthy throughout the 21-day observation period
and did not have detectable levels
of antibodies on 21 DPI; only one pigeon yielded the NP emu/TX
H7N1 on 3 DPI. The virus
was isolated from a tracheal swab and was believed to be the
residual inoculum virus. Based
on the responses of pigeons to NPAIV and HPAIV, it was
concluded that the pigeons were
resistant or minimally susceptible to infection with HPAIV
or NPAIV.
|