Black spot in canaries
Lessons from pigeons and
parrots
door: Dr. Jan Vanderborght, MD
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Most of us have been confronted in the past
with ‘black spot’ chicks. Chicks dying in their first days of life. Many have
tried to solve the problem, mostly without success. Every time we hear vets
speaking on a meeting, we all hope to hear what can solve this problem. But it
is not that easy. Let me take you on a journey, trying to understand better
what is going on.
Introduction
A virus is a
biological agent that reproduces inside the cells of living hosts. When
infected by a virus, a host cell is forced to produce thousands of identical
copies of the original virus at an extraordinary rate. Unlike most living
things, viruses do not have cells that divide; new viruses are assembled in the
infected host cell.
Also our canaries
face virus infections, best example being the pox virus, but there are many
others. Of one of these, the circoviruses, most scientists agree they are the
causative agent of what we call ‘black spot’.
Circovirus
infections are commonly associated with immune deficiency-related diseases that
are potentially fatal. A condition known as ‘black spot’ of neonatal canaries,
characterized by abdominal enlargement, gallbladder congestion and failure to
thrive, has been described for many years in Europe and was reported to have
been caused by a circovirus (Goldsmith, 1995). More recently, a circovirus-like
infection of canaries was identified in adult birds that had died following a
short illness characterized by dullness, anorexia, lethargy and feather
disorder (Todd et al., 2001).
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Foto 1 ● Veterinary center Trigenio – Nijlen
Dr. Coutteel
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Not much research
has been done on the canary circovirus (CaCV), probably because of being of no
economic value. Nevertheless, DNA analysis has been done, which showed the CaCV
is distinct from other circoviruses (parrots, pigeons, Gouldian finches,). This
means the virus is host specific, in a way CaCV cannot infect parrots or
pigeons or vice versa. But DNA analysis has shown the CaCV is closely related
to the pigeon circovirus (CoCV, 63,4% same DNA as CaCV) and the parrot
psittacine beak and feather disease (BFDV,62,9% same DNA as CaCV). (Phenix et
al., 2001)
In this
contribution I am making a hypothesis about what happens with black spot in
canaries, using some data coming from research which has been done in parrots
and pigeons. Future research will have to be done to prove or discard these
assumptions.
Observations
made
In canaries we
know chicks born with what we call ‘black spot’ show high mortality, up to
90-100%, due to secondary infections. This means the circovirus, which attacks
the immune system of the birds, makes the birds vulnerable to infections which,
under normal circumstances, pose no problem for the immune system of the birds.
Chicks die in their firsts days of life and as they are born with the ‘black
spot’, it seems infection already took place in the egg, before the chicks were
born.
In pigeons the
clinical picture of the ‘young pigeon disease complex’ is somewhat different.
Pigeons are affected between 1 month and 1 year of age, but it seems when they
are born, no problems are seen (Woods et all, 2000).
In parrots, the
psittacine beak and feather disease (BFDV), birds are infected between 2 months
and 3 years of age. The younger the birds are infected the more fatal the
clinical course (Miesle J., 2017)
For a review of
circovirus infections in non-psittacine birds I refer to Dr. Leslie Woods
(2000).
Birds develop
their immune system (antibody diversity) between the age of 3-6 weeks in the
Bursa of Fabricius. Birds infected before that age will never develop a mature
immune system and will die of secondary infections. Birds which are infected at
a later stage mainly show feather abnormalities.
In looking at
these different clinical pictures of related circovirus infections in different
breeds an important question arises. Why are parrots or pigeons not born with a
black spot, just like infected canaries do?
For answering this
question, we must know some things. In birds antibodies from the hen are
transferred to the egg. These antibodies (Ig Y in the yolk, IgA and IgM in the
egg white) do protect the just born chicks from a range of diseases in their
first days of life. Nature has created this because the immune system in not
yet fully developed. So, this very vulnerable ‘gap’ of let’s say 3 weeks after
hatch, has to be covered by these antibodies the chick has received from the
mother through the egg.
If we think this
way it seems logic pigeons and parrots must have received protective antibodies
from their mother in the egg, protecting them from circovirus infections in the
egg and in their first weeks of life.
As Dr. Leslie
Woods notes (2009): ‘Birds exposed to
BFDV (parrot circovirus) have been shown to seroconvert (produce protective
antibodies). Clinically normal birds that have been exposed to BFDV have higher
titers (number of antibodies) than birds with active infections, suggesting
that antibody is protective against development of clinical disease.
Experimental vaccination studies have demonstrated that chicks from vaccinated
hens remain clinically normal following challenge with BFDV’.
In the same way we
may think most of our canaries also have received protecting antibodies from
their mother through the egg. I say this because most of our canaries do not
have any problem with black spot.
If we would agree
this way of thinking is correct we immediately think: why? Why do some canary
hens do not provide their eggs with protective antibodies? If we agree most
birds are immune competent, the only reason can be: they have not been infected
before. For this we have to consider in which way circovirus infections are
transmitted.
Different
ways of transmission
Most scientists
agree the most important infection route is the horizontal way (from one bird
to another; feco-oral, feather dust). As the circovirus survives very well in
the surroundings and is very resistant to disinfection (in the way we do it) I
think most of our birds are infected in summer or winter. At this age they do
have a competent immune system and they develop protective antibodies, which
clear the body from the virus. In pigeons it has been shown 70% of the pigeons
do have protective antibodies in their serum (Stenzel, 2017).
Vertical
transmission (from mother to the egg) has been proven in pigeons and parrots,
but probably because of having protective antibodies infections in the egg, black
spots, just like in canaries, neonatal infections are not often seen.
In pigeons it also
has been noted transmission through sperm can occur (Duchatel 2009), so
probably this is also possible in our canaries. But as observations by canary
breeders show, this is not often the case.
Timing of
first infection
So, what happens
in canaries?
If the first
infection (primo infection) of canaries coincides with the start of the
breeding season black spot will pop up. If a bird gets infected by a virus
infection it takes some weeks to build the protective antibodies. If a hen lays
eggs in the meantime, the virus will be transferred to the egg without these
protective antibodies. As the hen is not yet cleared from the virus, the virus
will replicate in the egg, destroying the immune system, and whatever secondary
infection will kill the newly hatched chick. This is probably the reason why
black spot is seen more often in the first clutch of a breeding season. As the
breeding season progresses these hens will build more protective antibodies
which they can pass to their eggs.
Dr. Rob Marshall
(2005) notes: ‘Black spot occurs more
commonly in nests with a first-time mother’.
This seems to
support the hypothesis protecting antibodies are built as birds age.
It is also important
to note transfer of these protective antibodies differs even within the same
clutch (Speer Brian 2016). Late eggs in the laying order have less antibodies,
so protection is lower. In Nature this is compensated by higher levels of
testosterone in these eggs, so these chicks have higher competitive skills once
hatched. This could explain why some chicks in one nest do have black spot, and
other don’t.
Immediately we
pose ourselves the question: why are these hens infected at the start of the
breeding season? The answer could be easy: infection can occur all year round.
But this is not true. In pigeons we know circovirus infections alone are not
enough to produce disease (Schmidt 2008), so other factors are needed. One of
these is stress. It is well known stress paralysis the immune system. In
pigeons the first flights, basketting them and transport do cause stress. This
stress increases the stress hormone cortisol in the blood and gives rise to
immune suppression. This is why the ‘young pigeon disease’ pops up at this
time.
The start of the
breeding season always brings stress in the breeding room. Birds are located on
other places, hens becoming nervous, cocks challenging the hens and even the
longer daylight hours do produce stress and give rise to immune suppression.
Suppression of immunity during breeding season
In passerine birds
also something else comes along, and I quote Dr. Koutsos and Dr. Klasing (2014):
For example, a large body of evidence indicates
that high reproductive effort in female passerines suppresses indices of
cellular immunity and is often accompanied by decreased resistance. However, it
has been difficult to determine the extent to which immunosuppression is a
result of sex hormones versus changes induced by an elevated workload and
associated higher glucocorticoids, tissue damage and energy expenditure.
So, it seems apart
from the stress hormone cortisol, also the increased sex hormones do cause
immune suppression. Note this is only seen in passerine birds!
Interplay of different factors
Now we know
important factors are: protecting antibodies from the hen transferred to the
egg, and the timing of the primo infection are important, but this is not all!
As Prof. Dennis
Rubbenstroth, Institut für Virologie, Universitätsklinikum Freiburg (2016) says
about the young pigeon disease (YPD):
If YPD is an infectious disease the causative
agent(s) remain(s) still undiscovered.
It seems there is
a delicate interplay of 3 factors: circovirus – immune system (stress) –
secondary infections.
Only one of these
cannot cause the young pigeon disease. Experimental infection of pigeons with
circovirus did not cause disease. It is even thought circovirus infections
probably have been existing for a long time. They can be predisposing, but not
the real trigger. Do we have some other factors weakening the immune system,
like inbreeding or mycotoxins? Or, do we
have a problem with the secondary infections? For example, have E. Coli
infections become more virulent in time? We know these bacteria have become
more resistant to antibiotics, but this is not the same as virulence. I only
mention E. Coli, best known, but secondary infections can be caused by whatever
bacteria, viruses, fungi or protozoa.
An
impaired ability to absorb and ulitize yolk sac material has been noted in
black spot chicks (Dr. Coutteel, personal communication). In this way the chick
can not utilize the protecting antibodies from the yolk sac. As to the cause of
this inbreeding and breeding for new colour mutations have been proposed (Speer
2016).
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Foto 2 ● Veterinary center Trigenio – Nijlen
Dr. Coutteel
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What we can do
If one looks at
the three factors involved, each of them is important as to prevention and
understanding the disease.
Immunity
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A
variety of nutrients modulate the immune system. For example, several essential
nutrients fed at dietary levels that are clearly above the nutritional
requirement regulate the type of response to a pathogen that occurs, including
long-chain polyunsaturated fatty acids (PUFA) and vitamins A, D, and E.
Additionally, some nutrients that are not normally considered as dietary
essentials may modulate immunity, including carotenoids, phytonutrients (e.g.,
essential oils, genistein, cinnamaldehyde, curcumin, capsicum), and vitamin C.
As to secondary infections we could use probiotics (live bacteria), or
prebiotics like mannan oligosaccharides from yeast cell walls which have been
shown to reduce enteric E. Coli load.
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A
special note should be made about the use of beta-glucan. There has been one
study in which the use of beta-glucan has shown to clear the blood of parrots
from circovirus load. I quote Dr Tomasek (2008):
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Therefore, one of the possible
mechanisms of effect of b-glucan could be augmentation of interferon
production. This immune-stimulating substance is one of the promising solutions
in the fight against infectious diseases in poultry and other
animals; however, further investigation is needed to validate its efficiency in
psittacine birds.
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As
interferon therapy has been successfully used in parrots (Miesle 2017), this
could be true.
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Levamisole,
used as dewormer also has immune stimulating effects, but only at low dose.
Levamisole seems to have little effect on the normal immune system, but it
seems to stimulate a subnormal response and suppress hyperactive responses. The
effects are dose related. Low doses are reported to enhance responses, and
higher doses are reported to suppress responses (Lunn, 2004)
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I
want to mention an anecdotal story (Miller, 2010) about the use of carrot
juice. He pretended pigeons suffering from young pigeon disease were cured with
diluted carrot juice. If this can be reproduced or if it is true high level of
carotenoids can cure the birds remains to be proven. But the use of carrot soup
is also mentioned by Prof. Rubbenstroth (2016).
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But,
with all immune stimulants I want to quote Dr. Chalmers (2004):
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A general word of caution in the use
of immune stimulants: It seems to me that there have to be limits to the amount
of stimulation the immune system can handle before it collapses under the
strain of attempting to respond to multiple stimulating products. For this
reason, I’d suggest limiting the number of immune stimulants to only a few to
avoid exhausting the system.
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Immune
stimulation, OK, but at low dose and intermittent.
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Best
option would be vaccination, still unavailable till today. Maybe in the future
a vaccine will be produced using recombinant DNA. If we are lucky the targeted
fragments of the virus are the same for parrots, pigeons and canaries this
would be the ultimate answer.
Secondary infections,
prototype: E. Coli
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E.
Coli is a normal inhabitant of the birds intestinal flora, but is has been
shown domesticated birds do have higher levels in their intestines to their
wild relatives.
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Reducing
E. Coli: prebiotics, probiotics, hygiene protocol. Addition of 5-10% of egg
yolk powder also has shown to reduce E. Coli numbers, probably because of the
protective antibodies they contain (Kunert et all. 2015)
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The
use of oregano oil has proven to reduce enteric E. Coli (Sienkiewicz, 2012).
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Antibiotics.
Secondary infections can be eliminated by the use of antibiotics in a
successful way. Condition is these will have to be provided a few weeks before
the breeding season. In this way they can be loaded in the egg yolk (weeks
before egg deposition) and the egg white (24 hours before egg deposition) and
combat the secondary infections already present in the egg. The question is: do
we have to medicate all of our birds for these low numbers of black spot
chicks? And, even more important, using these will build antibiotic resistance
and a possible massive outbreak of black spot can occur the next year. Without
antibiotics we can see which chicks are ill, so we can cull them.
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Some
people will say they don’t want to lose all their chicks to black spot. But in
the case massive losses are met due to black spot it is my conviction the whole
shed is contaminated with multiple resistant bacteria (prototype: E. Coli) in
the intestines. One has to consult a vet for identification of which kind of
infection has come along and an antibiogram has to be made in search for the
correct antibiotic which clears the birds from these bacteria. In this case a
veterinary correctly prescribed antibiotic cure pre-breeding is 100% indicated
and will stop these massive outbreaks.
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One
final remark about antibiotics. It seems the fancy is leaving the (ab)use of
antibiotics, which is the way to go. So, most of us only give some preventative
as to coccidiosis. I read a comment by Dr. René Becker (2012):
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Caution should be exercised in using
Coccidiosis medicine, we made bad experience by using Baycox to many times.
Although highly active against coccidia, it is not uncommon after treatment to
get outbreaks of youngsters disease.
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I
have been searching for this on medical databases but did not find any proof
Baycox compromises our bird’s immune system. Remember Baycox only combats
coccidiosis but not whatever bacterial infection. It is my idea in the past we
all used products like ESB3 30% pre-breeding for controlling coccidiosis. But
ESB3 30% is a sulfamid antibiotic which also kills E. Coli in the intestines,
so secondary infections become less frequent. Due to increased antibiotic
resistance this way of doing things would not work any longer.
Circovirus
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As the
circovirus is very stable and can persist for months or even years it is hard
to get rid of it. Some disinfectants like F-10 or Virkon S can kill the virus,
but enough contact time or repeated use has to be done to achieve low levels
(Stanford, 2006; Australian Government 2006). Heat disinfection by using steam
cleaners is also a possibility. Temperature needed is 90°C for 5 minutes
(Emmoth, 2014). Using heat steaming also has the advantage red mite eggs are
killed, as they are already killed at temperatures above 40°C. This is very
important because red mite eggs can survive for months in the surroundings and
are not killed by commonly used sprays.
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It is
even a question if total disinfection would be wise, as for natural build-up of
antibodies in immune competent birds the virus has to be present.
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As the
circovirus is the smallest known DNA virus it can also attach itself to dust,
so good ventilation is very important.
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Culling
black spot chicks must be done. One can try to save black spot chicks, and this
has been done often by the use of fluids and/or antibiotics it seems to me
these chicks will never have a fully developed immune system, and these birds
probably will become carrier birds without producing antibodies. They will keep
on spreading the virus, and if they survive the virus will be silently present
in the genital tract as long as they live.
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The same
holds true for hens having black spot chicks in the second or third clutch.
These hens have not produced protecting antibodies and are the silent carriers
of the virus.
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Buying
birds can always pose a problem. But don’t blame the seller too soon if black
spots pop up. It could be possible you bought a bird carrying the virus, but if
it fit looks healthy nobody knows. It is also possible this bird is a carrier
of different serotypes of E. Coli.
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As we
know timing of infection is important. The younger the birds are at the time of
infection the more pronounced the effects as to mortality. At a very young age
immune suppression dominates the picture with birds dying of even banal
secondary infections. At later ages,
plumage deformities dominate the picture.
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But if
you already experienced black spot in your shed, and you have a bird with some
chronic feather problems (mainly the long tail and wing feathers) it is almost
certain this is a circovirus shedding bird, which has to be culled.
Conclusion
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Black
spot is no disaster, except for massive outbreaks, which seem to be the
exception rather than the rule. Till today no vaccine is available.
Understanding the disease is very important as to prevention and/or
interpretation of what we see.
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As the
disease seems multifactorial, just like in pigeons, we propose to call it ‘black
spot disease syndrome’.
‘Black spot disease syndrome’ would
reflect better the phenomenon of black spot we observe.
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Dr. Jan
Vanderborght MD
January 2018
Thanks to Dr. Coutteel DVM and Ing. Vanden Borre Msc, for their specific
contribution.
References
·
Becker René (2012): Ask the Vet, Young Pigeon disease.
http://www.amazing-wings.com/index.php/en/12-fragen-an-rene/89-ask-the-vet-young-pigeons-disease-what-to-do
·
Chalmers (2004): 75th annual meeting of the Canadian Racing Pigeon Union
and the 100th anniversary of the Calgary RPC, held in Calgary, Alberta, Canada
·
Duchatel Jean Pierre(2009). Quantification of pigeon circovirus in
serum, blood, semen and different tissues of naturally infected pigeons using a
real-time polymerase chain reaction. Avian Pathology, Taylor & Francis,
pp.143-148
·
Emmoth et all. (2014): Heat inactivation of porcine circovirus type 2.
·
Goldsmith, T. L. (1995). Documentation of passerine circoviral
infection. In Proceedings of the Annual Conference of the Association of Avian
Veterinarians, pp. 349–350, August 1995, Philadelphia, PA, USA
·
Hygiene Protocols for the Prevention and Control of Diseases
(Particularly Beak and Feather Disease) in Australian Birds (2006) Australian
Government Department of the Environment and Heritage
·
Koutsos and Klasing† (2014): Factors Modulating the Avian Immune System
·
Kunert Filho et all. (2015) Avian Pathogenic Escherichia coli (APEC) -
an update on the control.
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Lunn et all. (2004): Immunomodulation: Principles and Mechanisms. 50th
Annual Convention of the American Association of Equine Practitioners,
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Marshall Rob (2005): Canary Health
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Miesle J. (2017) Psittacine Beak and Feather Disease. An Overview
In: IVIS Reviews in Veterinary Medicine,
I.V.I.S.
·
Miller Garry (2010) Arizona Pigeon Club
http://www.aviculture-europe.nl/nummers/10E01A09.pdf
·
Phenix et all. (2001)Nucleotide sequence analysis of a novel circovirus
of canaries and its relationship to other members of the genus Circovirus of
the family Circoviridae. Journal of General Virology
·
Schmidt V., Schlomer J., Luken C., Johne R., Biere B., Muller H.,
Krautwald-Junghanns M.-(2008).: Experimental infection of domestic pigeons with
pigeon circovirus. Avian Dis. 52,
380-386.
·
Rubbenstroth Dennis, DVM, PhD (2016) FCI Meeting, Halle: Update on „Young pigeon disease (YPD)
syndrome“
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Sienkiewicz (2012): The antibacterial activity of oregano essential oil
(Origanum heracleoticum L.) against clinical strains of Escherichia coli and
Pseudomonas aeruginosa
·
Speer Brian (2016) Current Therapy in Avian Medicine and Surgery
·
Stanford (2006) Control of circovirus infection in psittacine birds
using F-10 disinfectant and avian gamma interferon
·
Stenzel et all. (2017) Application of pigeon circovirus recombinant
capsid protein for detecting anti-PiCV antibodies in the sera of asymptomatic
domestic pigeons and the potential use of a combination of serological and
molecular tests for controlling circovirus infections in pigeon breeding
flocks.
·
Todd, D.,et all. (2001). Nucleotide sequence identification of a novel circovirus
from canaries. Avian Pathology 30, 321–325
·
Tomasek (2008) Psittacine Circovirus Infection in Parakeets of the Genus
Eunymphicus and Treatment with β-(1,3/1,6)-D-Glucan
·
Woods et all. (2000): Circovirus Infection of Nonpsittacine Birds
Journal of Avian Medicine and Surgery
·
Woods (2009) Diseases of poultry: Circovirus infections of pigeon and
other avian species.
