Manual of Pigeons Diseases

Manual Of Pigeons Diseases Dr.
Ali Kareem
Manual of Pigeons Diseases

Dr. Ali Kareem Al-Saeidi
‫‪Manual Of Pigeons Diseases‬‬ ‫‪Dr. Ali Kareem‬‬
‫اﻟﻜﺘﺎب ﻣﺄﺧﻮذ ﻣﻦ ﻋﺪة ﻣﺼﺎدر وﺗﻢ اﻗﺘﺒﺎس اﻟﻤﻌﻠﻮﻣﺎت ﺑﺎﻻﻋﺘﻤﺎد ﻋﻠﻰ اﻟﺨﺒﺮة اﻟﺸﺨﺼﯿﺔ‪،‬‬
‫وﺑﻌﺾ اﻟﻤﺼﺎدر اﺧﺬ ﻣﻨﮭﺎ اﻟﺼﻮر ﻓﻘﻂ‪.‬‬
‫ﻣﻼﺣﻈﺔ ھﺎﻣﺔ ‪ :‬ﯾﺴﻤﺢ ﺑﻨﺸﺮ اﻟﻜﺘﺎب ﺑﻜﺎﻓﺔ أﺷﻜﺎﻟﮫ اﻹﻟﻜﺘﺮوﻧﯿﺔ ﻋﺪا اﻟﺸﻜﻞ اﻟﻤﻄﺒﻮع ﻣﻨﮫ ‪،‬‬
‫ﺣﯿﺚ ﻻ أﻋﻄﻲ أي ﺟﮭﺔ ﻛﺎﻧﺖ ﺣﻖ طﺒﺎﻋﺔ اﻟﻜﺘﺎب أو ﺟﺰء ﻣﻨﮫ ﺑﺄي ﺷﻜﻞ ﻣﻄﺒﻮع ﻛﺎن‪.‬‬
‫د‪ .‬ﻋﻠﻲ ﻛﺮﯾﻢ‬

Manual Of Pigeons Diseases Dr. Ali Kareem
List of Contents
Section No. Content Page No.

List of Contents
Section No. Chapter One: Viral Diseases Page No.
1 Paramyxovirus infection
1
2 Pigeon circovirus infection
5
3 Pigeon adenovirus infection

7
4 Necrotizing hepatitis (adenovirus type II(
9
5 Pigeon herpes virus infection
9
6 Pigeon Pox
11
Section No. Chapter Two: Bacterial Diseases Page No.
1 Salmonellosis
15
2 Chlamydophilosis (ornithosis(
18
3 Streptococcus gallolyticus infection
20
4 E. coli (Collibacillosi(
22
5 Staphylococcal
23
6 Pasteurella Multocida
24
7 Mycoplasma
25
Section No. Chapter Three: Protozoa & Fungal Page No.
1 Protozoa diseases
2 Trichomoniasis (canker)
27
3 Spironucleus columbae (hexamitiasis(

29
4 Coccidiosis
29
5 Haemoproteus spp
31
6 Fungal diseases
7 Aspergillosis
32
8 Candidiasis
33
Section No. Chapter Four: Parasitic diseases Page No.

1 Worm infections
2 Helminths
34
3 Roundworms
34
4 Hairworms (threadworms (
35
5 Stomach worms
35
6 Tapeworms
35
7 Strongylids
36
8 Ectoparasites
9 Fleas
37
10 Mosquitoes
37
11 Lice
37
12 Parasitic Mites
37
Section No. Chapter Five Page No.

1 Nutritional disease
2 Vitamin deficiencies and toxicosis: 40

3 Vitamin B deficiency
40
4 Vitamin D deficiency
41
5 Mineral/electrolyte deficiency or
overdosage 42
6 Calcium and phosphorus

42
7 Sodium, potassium and chloride
42
8 Magnesium
43
9 Iodine
43
10 Malnutrition and loss of performance 43
11 Intoxication with feed or medication
44
12 Mineral toxicosis 45
13 Drug overdosage 45
14 Poisoning
46
15 Mycotoxins
47
16 Organophosphates
48
17 Insecticides 48
Section No. Chapter six: Other diseases Page No.
1 One-Eyed Cold
51
2 Sour Crop
51
3 Haemochromatosis
52
4 Visceral gout
53
5 Articular gout
54
Section No. Chapter seven: Breeding & Racing Page No.

1 1. Normal breeding
55
2 2. Diseases associated with Breeding

56
3 3. Infertility
56
4 4. Embryonic mortality
59
5 5. Contamination
59
6 6. Racing season
60
7 7. Resting period
61
Section No. References 62

Chapter one: Viral Disease:
1. Paramyxovirus infection
2. Pigeon circovirus infection
3. Pigeon adenovirus infection
4. Necrotizing hepatitis (adenovirus type II(
5. Pigeon herpes virus infection
6. Pigeon Pox
Paramyxovirus infection:
 Avian paramyxoviruses can be divided into nine different serotypes, the most
important of which is paramyxovirus serotype 1 (PMV-1), the causal agent of
classic Newcastle disease in poultry.
 When this was causing heavy losses in the UK poultry industry in the 1970s the
virus occasionally spread to pigeons, causing depression, incoordination, leg and
wing weakness, twisted necks and death.
 Disease in pigeons was, however, unusual and represented a spill-over of classic
Newcastle disease from poultry. In 1977 a 'new' disease struck pigeons in Iraq,
spreading to Egypt in 1978. Italy in 1981 and Sudan in 1982. This disease caused
depression, muscle tremors, loss of appetite, abnormal head carriage, circling,
paralysis of the wings or legs, diarrhoea and high mortality. A viral cause was
suspected and initially suspicion fell on pigeon herpesvirus. Eventually it was
shown that the causal virus was PMV-1, but a variant strain that was slightly
different from the classic Newcastle disease virus. This variant strain is now
referred to as pigeon PMV-1, or PPMV-1, and can be differentiated from
classical PMV-1 using a panel of monoclonal antibodies.
 Disease in pigeons spread through Europe in 1982 and reached Great Britain in
1983. PPMV-1 has also periodically spread from pigeons to poultry flocks and
game birds, and so the disease in pigeons has been made notifiable.
 In addition, because of the risk that pigeons may become a reservoir of infection
for poultry flocks, all pigeons being raced or shown must be vaccinated against
PPMV-1.
Epidemiology:
 PPMV-1 has been found in wild birds such as feral pigeons, woodpigeons and
collared doves.
 Racing pigeons and show pigeons may be exposed to PPMV-1 through direct or
indirect contact with infected wild birds or by contact with infected racing
pigeons during training, racing or showing.
 Vaccinated birds may pick up the virus on their feathers and feet and transport it
back to the loft, infecting unvaccinated birds such as young birds or breeding
birds. Birds bred late in the season may be particularly vulnerable because such
birds are often left unvaccinated for a longer period.
 Immunosuppressive conditions of young birds such as pigeon circovirus infection
may predispose to PMV infection or reduce the response to the PMV vaccine.
Even healthy birds vaccinated against PPMV-1 may succumb to disease if the
viral challenge is sufficiently high.
1
 Unlike certain other diseases, infected birds do not become lifelong carriers but
stop excreting virus within 6-8 weeks of the initial infection.
Clinical signs:
a. Clinical signs can be seen as early as 5 days after picking up the virus, or as long
as 6 weeks after acquiring infection.
b. PPMV-1 causes an interstitial nephritis, resulting in polyuria in a high proportion
of susceptible birds.
c. The birds drink more than normal and produce watery green faeces consisting of
a pool of clear urine surrounding a core of green material.
d. Fanciers often comment that the floor of the loft becomes very wet and describe
the faeces as 'green diarrhoea', but the wet green faeces result from a combination
of polyuria, polydipsia and increased excretion of bile.
e. When the disease was first seen in the 1980s nervous signs were frequently
observed, such as loss of balance, inability to pick up feed, torticollis, unilateral
or bilateral paralysis of legs or wings, loss of righting reflexes, circling,
somersaulting, attempting to fly backwards, or tremors of the head and neck
(Figure 1&2).
f. Mortality In adults was usually low, but could be high in young birds as a result
of secondary malnutrition or kidney failure.
g. In recent years the pattern of clinical signs appears to have changed, with higher
mortality in some outbreaks and smaller numbers of birds showing nervous signs.
h. In general, most birds continue to eat and weight loss is not severe. Recovery
from the diarrhoea and mild nervous signs can take 3-8 weeks. The outcome in
birds with severe nervous signs cannot be predicted but some birds eventually
recover.
A B
Figure1: A- Torticollis In a pigeon with PPMV-1 infection. B- Balance disorder.
2
Figure 2: Paramyxovirosis (PMV1). Balance disorder.
Post-Mortem Findings:
There are no specific lesions in pigeons apart from generalised congestion of the
viscera which indicates a septicaemia.
Diagnosis:
History and clinical signs. Confirmation requires serology (haemagglutination
inhibition test) and virus isolation. Serological diagnosis is more difficult in birds
that have been vaccinated against pigeon paramyxovirus infection.
Differential Diagnosis:
Should include chlamydiosis, poisoning and other systemic infections.
Treatment:
a. Different countries have different strategies for the control of this disease, but in
suspected presence of PPMV-1 and birds must be prevented from flying out.
b. If disease is confirmed, movement of pigeons into or out of the loft will be
prohibited for at least 60 days.
c. Electrolytes in the drinking water are beneficial, and birds with neurological signs
should be placed in small groups and assisted to feed and drink.
d. Severely affected birds should be culled if they do not show any signs of
improvement within 2 weeks. Hygiene and the efficient use in the loft of
3
approved disinfectants are essential to limit the spread of PPMV-1 and to control
secondary conditions.
Control:
a. In general terms young birds should be vaccinated against PPMV-1 from 3-4
weeks of age onwards, and adults 3-6 weeks before the onset of breeding, racing
or showing. Annual re-vaccination is required. If using the combined PMV-pox
vaccine, vaccination of young birds should be delayed to 6 weeks of age.
b. Vaccine is administered by subcutaneous injection in the lower part of the neck.
c. A very small proportion of birds may develop small lumps or large subcutaneous
abscesses. These reactions will be minimized by using good hygienic practices
when vaccinating birds.
d. Very rarely a bird may collapse and die shortly after vaccination; at post-mortem
examination the blood vessels under the skin of the neck are found to be engorged
with blood. This adverse reaction is probably due to the unusually rich blood
supply to this part of the neck, with many tiny veins and sinuses, especially in
cock birds.
e. Such adverse reactions can be minimized by vaccinating at the base of the neck
rather than behind the head, with the neck stretched out and the needle pointing
towards the tail of the bird.
Feature Comment
Percentage of birds with diarrhoea.. Much higher in PMV-I
Percentage of birds with nervous signs. Much higher in PMV- 1.
Nature of diarrhoea. Excess watery urine in PMV-I .Soft, slimy,
bulky in paratyphoid.
Nature of nervous signs. Become more pronounced in PMV-I when the
bird is stressed.
Loss of weight. More severe in paratyphoid.
Loss of appetite. More severe in paratyphoid.
Swelling of joints. Swelling of joints. A feature of paratyphoid, not
of PMV-I .
Mortality in squabs. Much higher in paratyphoid.
Table 1. A comparison of the clinical signs of PMV-l and salmonellosis (paratyphoid).
4
Pigeon circovirus infection

a. 'Young bird sickness' is a common syndrome of young racing pigeons, usually
seen between the ages of 4 weeks and 4 months.
b. Affected birds are lethargic, with loss of appetite, the production of green watery
faeces, and sometimes retention of food in the crop.
c. Many birds return to health within 5-7 days but some deteriorate, resulting in the
death or culling of the bird.
d. The cause or causes of this syndrome probably vary with time, but currently a
primary circovirus infection with other secondary infections is thought to be one
of the major causes.
Epidemiology
a. Most circoviruses target the immune system of the host and this appears to be
true tor pigeon circovirus, which attacks the bursa of Fabricius, making birds
more susceptible to infectious disease and reducing their ability to respond to
vaccines.
b. The bursa is only active in young birds and regresses as the birds mature.
c. No evidence was found that crop milk was a major route of transmission. These
studies also detected viral DNA in blood and cloacal swabs from a high
proportion of young birds, including healthy birds, and sequential studies
suggested that most young pigeons became infected between 2 and 10 weeks of
age and then continued to excrete the virus.
d. These findings suggest that carrier adults are present in lofts and that some young
birds become infected from their parents, with subsequent direct and indirect
spread to other young birds.
Clinical signs ('young bird sickness')
a. Circovirus infection has been demonstrated in birds showing signs such as ill
thrift, loss of appetite, weight loss, 'diarrhoea' or poor racing performance.
b. Less commonly, signs of vomiting, respiratory disease or central nervous signs
are seen.
c. The role of circovirus in 'young bird sickness' remains to be proven, and it is
difficult to separate out the primary effects of the virus and the results of
immunosuppression and secondary diseases.
5
d. The nature and severity of the clinical signs will vary depending on the secondary
infections, and mortality approaching 100% has been reported in a few severely
affected lofts.
Diagnosis
a. Circovirus DNA can be demonstrated by PCR in tissues, cloacal swabs and blood
samples from infected birds.
b. Viral DNA can also be detected in apparently healthy birds, therefore additional
evidence is required to establish the significance of positive results and tests for
other pathogens should be carried out.
c. Gross post-mortem examinations of birds that have died or been culled usually
only show evidence of a range of secondary infectious diseases, but
histopathological examination typically reveals damage to the immune system.
d. Lymphoid depletion commonly occurs in the bursa and also in spleen, caecal
tonsil and gut-associated lymphoid tissue. Some of the bursal follicles may be
almost devoid of lymphoid cells and may be cystic. Numerous
e. characteristic botryoid intracytoplasmic inclusions are seen within the
macrophages of the bursa, especially in the medulla but also in the cortex.
Treatment
a. There is no specific treatment for circovirus infection, and it must instead be

supportive and aimed at controlling any secondary infections identified at
postmortem examination.
b. Feeding a light diet and the addition of electrolytes to the drinking water may be
beneficial.
c. It has been suggested that cider vinegar in the drinking water for 5 days may help
to control secondary yeast infections in the crop, and a probiotic or live yoghurt
may help to restore the normal intestinal bacterial flora.
Control
 The mechanics of pigeon racing make it likely that young birds will at some time
be exposed to this virus. If the birds are only exposed to small numbers of
viruses, and if they are not subjected to other stresses or pathogens, clinical signs
may be minimal or absent.
 Control must therefore focus on keeping virus numbers in the loft and pigeon
transporters to the minimum and on reducing stress factors.
 Controlling other conditions, such as paramyxovirus and trichomoniasis, will
reduce the likelihood of secondary involvement of such pathogens.
6
Pigeon adenovirus infection
 Inclusion body hepatitis associated with an adenovirus infection became a

significant cause of disease in young racing pigeons in continental Europe in the
1980s and 1990s.
 In the summer of 1993 there was a marked increase in the number of cases of
adenovirus infection in young pigeons in the UK, referred to as 'young bird
sickness', the 'vomiting syndrome' or 'adenovirus type Pi This form of 'young bird
sickness' has become less common again in the UK and has been replaced by a
'young bird sickness' associated with pigeon circovirus.
 In addition, a severe necrotizing hepatitis associated with an adenovirus and
affecting pigeons of all ages has been described in continental Europe
(adenovirus type II).
Epidemiology:
a. The 'classical' form of adenovirus inclusion body hepatitis characteristically
affects young birds under a year old.
b. Disease may be seen before the onset of young-bird racing, but outbreaks
commonly occur a few days after the birds return from racing.
c. It seems likely that the stress of being transported to the race site and possible
delays before liberation increase excretion of the virus and subsequent spread
to other birds in the basket, with further spread to other young birds in the loft
when the infected birds return home.
d. Damage to the intestine and crop, intestinal stasis and alterations to the normal
flora of the alimentary tract may result in secondary overproliferation of
bacteria and yeasts, most often E. coli and Candida albicans.
e. Infection is acquired through the oral-faecal route. Vertical spread is important
in some adenovirus infections of poultry but the significance of this route in
pigeons is unclear.
Clinical signs:
a. The adenoviruses damage the cells of the intestine and then the liver, resulting in
the production of green faeces, excessive drinking, vomiting, and failure of the
birds' crops to empty properly.
b. Most birds recover within 4-6 days but in those with secondary yeast infections of
the crop there may be substantial loss of weight, and death within 24 hours can
occur due to secondary E. coli septicaemia.
c. Recovered birds are often reluctant to exercise, and if such birds are sent training
or racing they may not be fit enough to return home.
7
Diagnosis:
a. A history of sudden onset of crop stasis, regurgitation and diarrhoea in birds a
few days after their return from racing is suggestive of adenovirus inclusion body
hepatitis.
b. Post-mortem examination is often unspectacular, but there may be a catarrhal

enteritis and moderate to marked hepatomegaly with haemorrhages and
occasionally pinpoint liver necrosis.
c. Evidence of concurrent infections such as crop candidiasis, trichomoniasis and

colisepticaemia may be found.
d. Confirmation of the role of adenovirus is based on the histopathological
appearance of the liver, in which significant numbers of large intranuclear
inclusions can be found in the hepatocytes, hence the name 'inclusion body
hepatitis'. The majority of the inclusions are basophilic, filling most of the
nucleus. Eosinophilic inclusions are seen less frequently, surrounded by a halo
and marginated nuclear chromatin, and may be confused with the eosinophilic
inclusions caused by herpesvirus infections.
e. Unlike infections with pigeon herpesvirus and adenovirus type II. Extensive liver
necrosis is not usually seen.
f. Attempts to isolate pigeon adenovirus are frequently unsuccessful, therefore

laboratories experienced with this virus should be chosen. A PCR that detects this
virus has been developed and is available in some countries.
Treatment and control:

See comments on the treatment and control of pigeon circovirus infection.
8
Necrotizing hepatitis (adenovirus type II):
a. A necrotizing hepatitis of racing pigeons associated with an adenovirus infection

has been described in pigeons in Belgium and neighbouring countries, affecting
birds of all ages.
b. Affected birds are severely depressed and die within 24—48 hours.
c. Vomiting and yellow diarrhoea may be seen prior to death and overall mortality
in the loft can be high - often 30% and sometimes even higher.
d. An enlarged pale yellow liver with a red sheen has been described at post-mortem
examination, and basophilic or eosinophilic intranuclear inclusion bodies can be
found on histopathology.
e. Unlike the classical inclusion body hepatitis, the inclusions tend to be relatively
small and few in number, but are accompanied by extensive hepatic necrosis.
Pigeon herpesvirus infection:
 Pigeon herpesvirus, related to but distinct from other avian herpesviruses, was
first described in the UK in 1964 and still causes problems in pigeons of all ages.
 The virus appears to be widespread in Europe, with one survey showing that over
60% of clinically normal pigeons had encountered the virus.
Epidemiology:
a. Some clinically healthy adult birds carry this virus, intermittently excreting it and
infecting their progeny and other in-contact birds.
b. Transmission of virus into the egg probably does not occur, but infected adults
shed virus in their faeces and from the oropharynx, passing virus to their
offspring during feeding.
c. The stress of rearing multiple rounds of young birds may increase viral shedding
as the breeding season progresses, resulting in further spread of virus to other
young birds in the loft. Once infected, birds may become carriers for life,
intermittently excreting the virus during periods of stress.
d. Clinical disease typically occurs when the birds are aged 1-6 months, possibly
after maternal immunity has waned. Clinical disease may follow the introduction
of purchased carrier birds to the loft, and disease has also been seen in feral
pigeons, providing another possible source of virus. Concurrent bacterial, viral,
9
yeast and trichomonad infections may be seen in birds with pigeon herpesvirus
infection.
Clinical Signs:
PHV is a common disease, particularly of young pigeons under six months of age:
Acute infection:
The following signs may be seen: sneezing; protruding membrana nictitans;
conjunctivitis; clear discharges from the nares with subsequent rhinitis; cere
tuming brown; congestion of the mucous membranes of the mouth; diphtheritic
membrane formation; occasionally ulcers (figure3). Other signs are more
indicative of a systemic infection. These include vomiting, diarrhoea, and
lethargy. The inability to fly and occasionally death.
Chronic infection:
The following signs may be seen: sinusitis; white spots on the soft palate;
dyspnoea and secondary complications due to bacterial infections (Escherichia
coli, Pasteurella spp, Staphylococcus spp. and Streptococcus spp.);
trichomoniasis; and Mycoplasma spp. infection.
Figure3: Pigeon herpesvirus: necrotic debris in the
10
Diagnosis:
a. Confirmation of the diagnosis is usually made at postmortem examination.
b. Plaques of necrotic debris may extend from the oral cavity to the crop and larynx.
c. The liver is often enlarged and mottled, sometimes with foci of necrosis and
haemorrhage. Pericarditis and airsacculitis may be present, and the intestine may
be distended with green fluid.
d. Histopathological examination of the liver typically demonstrates foci of

hepatocyte degeneration and necrosis associated with eosinophilic intranuclear
inclusion bodies.
Treatment:
 Nursing and supportive therapy are very important.
 This should include the provision of extra heat, antibiotic therapy and treatment
for trichomoniasis if necessary.
 Chemotherapy has been tried using trisodium phosphonoformate and
acycloguanosine, but it failed to prevent infection.
Control:
 The virus is most likely to be introduced to the loft by a carrier bird. New stock
should be obtained from reputable sources and ideally should undergo a period of
quarantine before being admitted to the main loft.
 Loft management should aim to minimize stress in the birds, thus reducing virus
shedding, and good loft hygiene is essential to limit herpesvirus numbers and to
control other infectious agents.
Pigeon Pox
Host
Pigeons are the natural host. Serological cross reactions can be demonstrated
between pigeon pox virus and fowl pox and falcon pox viruses.
Transmission
 This is primarily by direct contact via cuts and abrasions, ego fighting in race
baskets or insect bites. Respiratory infection could occur from aerosols in a
contaminated environment when the virus has been shed from infected feather
follicles and dried scabs. Infected parents feeding squabs will also transmit
infection. The incubation period is between 4-14 days.
 The virus is hed from infected pocks and feather follicles. In chickens a latent
infection has been demonstrated for 13 months.
11
Clinical Signs
a. Pigeon pox is a common disease of young pigeons.
b. The earliest signs are slight closing of one eye, excessive lacrimation and
development of a firm white swelling on the eyelid.
c. This rapidly enlarges, becoming more yellow to brown and crusty. Lesions may
also be found around the nares, the commissures of the beak, the pharynx and the
larynx. Occasionally, lesions may also be seen on the legs. An internal form can
also occur (Figure 4).
d. An atypical form of pigeon pox is also seen. Isolated cases or a sporadic outbreak
of 'warts', 'blood blisters' or 'protein bumps' may be presented.
e. These can be found on the leading edge of the wings, breast and rump. They can
vary in size from 5-25mm diameter. If damaged, they will bleed profusely. The
course of infection in both typical and atypical pigeon pox is approximately three
weeks. Scars may be left at the site of the pox lesion. In some cases, beak
deformities may occur (Figure 5).
Figure5:Atypical pigeon pox: large black Figure4: Pigeon pox (cutaneous form).
mass on the breast. Crusts on the eyelids and beak.
12
Figure 4: Diphtheroid form of pigeon pox. Figure4:: Pigeon pox (cutaneous form).
Post-Mortem Findings
Post-mortem examination confirms the extent of the lesions and whether or not
there has been any involvement of the oesophagus or trachea which has prevented
feeding or breathing.
Diagnosis
 The owner may report that the pigeons showed poor performance in a race two
weeks earlier. This, in conjunction with the clinical signs, is virtually
pathognomonic for pigeon pox.
 Isolation of the pox virus from pox lesions or direct electron microscopy will
confirm the diagnosis.
 Additional tests include histopathology - demonstrating the presence of Bollinger
bodies - and the agar gel precipitin test on pox lesions.
Treatment:
a. There is no specific treatment.
b. Surgical removal may be necessary if the lesion(s) interferes with vital functions.
c. Painting the lesions with aqueous iodine may be beneficial.
d. Antibiotics to control secondary infection may also be necessary to ensure that

the bird can feed and breathe. Concurrent trichomoniasis must be treated if
present, as this will exacerbate the condition.
e. In large lofts, where stock birds are kept separate from the race teams, it may be
decided to vaccinate the remainder of the birds.
13
f. Under no circumstances should vaccinated birds be allowed to race for at least six
weeks. Extreme caution must be exercised, especially if the stock birds are
rearing youngsters.
g. In uncomplicated cases the lesions of both typical and atypical pox will resolve
naturally.
Control:
a. A pigeon pox vaccine is available.
b. The vaccine is rubbed into plucked feather follicles on the leg.
c. Vaccine must not be allowed to get onto the hands as it might inadvertently be
transferred to the pigeon 's eye or mouth. Under no circumstances should vaccine
be applied to a bleeding feather follicle .
d. All the birds in the loft should be vaccinated at the same time. Annual boosters
are recommended .
e. Breeding stock should be vaccinated at least six weeks before pairing up and all
race birds should be vaccinated six weeks before the first race .
f. Only healthy birds should be vaccinated. Do not allow recently vaccinated birds
to mix with unvaccinated birds.
g. Following an outbreak, thorough disinfection of the loft is required. Steam
cleaning is particularly effective.
14
Chapter Two: Bacterial Diseases
1. Salmonellosis
2. Chlamydophilosis (ornithosis(
3. Streptococcus gallolyticus infection
4. E. coli (Collibacillosi(
5. Staphylococcal
6. Pasteurella Multocida
7. Mycoplasma
Salmonellosis
 Salmonellosis often referred to as 'paratyphoid' by pigeon fanciers, can result in a
wide range of presenting signs.
 Although there are over 2000 different serovars of Salmonella, the great majority
of isolates from racing, show and feral pigeons are Salmonella enlerica serotype
Typhimurium definitive phage types 2 and 99 (S. typhimurium DT 2 and DT 99).
Epidemiology:
a. Apparently healthy pigeons can carry this organism, intermittently excreting it in
their faeces.
b. Purchased birds, stray racing pigeons or feral pigeons could therefore bring
Salmonella into the loft, or the organism could be introduced after contact with
infected birds during training, racing or showing.
c. The fancier, visitors, vaccinating teams, etc. could also be the source of infection,
carrying the bacteria on contaminated clothing, footwear or equipment, and
rodents such as rats and mice could mechanically spread the organism from other
infected pigeon lofts.
d. Clinical disease may not be immediately apparent and some infected birds remain
as carriers.
e. Increased excretion may occur subsequently when birds are paired up for
breeding, carrier birds passing the organism into their eggs and 'crop milk' in
addition to the faeces, causing disease in the next generation of birds.
Clinical signs:
a. After ingestion of the bacteria and colonization of the intestine there is often
a bacteraemia or septicaemia, with subsequent localization of Salmonella
organisms in tissues such as liver, lung, spleen, pancreas, kidney, gonad and
joints.
b. Losses of appetite, green diarrhea (Figure 6) and increased mortality or

culling are typically seen, affecting all age groups.
c. Weight loss can be rapid and severe.
d. The fancier may report more 'clear' eggs than normal and increased dead-in-
shells and mortality in the first week of life.
e. A small proportion of the birds may develop abnormalities of the central

nervous system such as loss of balance, circling and lateral recumbency.
Some birds cannot hold their head in the normal position and have difficulty
in picking up their food.
15
f. In some birds the joints of the wings and legs may be hot, swollen and
painful, causing the bird to be lame or to droop a wing (Figure 6).
A A
A B
Figure 6:
A- Salmonellosis: swollen elbow joint. B- Diarrhoea in a pigeon with salmonellosis
.
Diagnosis
a. Feces, either from individual birds or pooled from the loft, can be cultured for the
presence of Salmonella.
b. Selective or enrichment media may be required, especially when screening fecal
samples.
c. However, because of the intermittent excretion of the organism, a negative fecal
sample does not rule out salmonellosis, and post-mortem examination of birds
that have died or been culled should be carried out.
d. Enlargement of the liver and spleen may be seen, sometimes with a purulent
pericarditis and perihepatitis. Pale foci of necrosis or granulomas up to 10 mm in
diameter in the liver, lung or Intestine are frequently seen, and less often in other
organs such as spleen, pancreas and kidney.
e. A purulent arthritis affecting one or more joints (especially the elbow joints) may
also be seen, and in some chronic cases there can be substantial periarticular
16
fibrosis. Bacteriology, including selective cultures for Salmonella, should be

made from a wide range of post-mortem tissues.
f. Similar to the situation with faecal examination, the causal organism may not be
readily demonstrated in all infected birds, and a combination of pooled faeces and
several dead birds may need to be examined before the diagnosis can be
confirmed.
Treatment:
a. All the birds in the loft should be treated with an appropriate antibacterial such as
amoxicillin or enrofloxacin, selected on the basis of an antimicrobial sensitivity
test.
b. Treatment should be given in the drinking water for at least 10 days, and
preferably for about 3 weeks, combined with thorough cleansing and disinfection
of the loft, feeders and drinkers.
c. This could be followed by a course of probiotics in the drinking water.

d. It is advisable to cull birds with swollen joints or showing advanced central
nervous system signs and those with severe weight loss.
e. Following treatment and loft disinfection, pooled faecal samples should be

screened for Salmonella on several occasions, including before the onset of
breeding, with a repeat of the treatment programme if required.
Control:
a. Good hygiene, avoiding overcrowding, obtaining new stock from reputable
sources and excluding stray and feral pigeons from the loft will help to reduce the
risk of salmonellosis. These measures should be coupled with routine screening
of pooled faeces, especially before the onset of breeding.
b. Vaccines (live and inactivated) against salmonellosis are used in some countries,
for example in adults before the onset of breeding in lofts that have previously
experienced problems with salmonellosis.
c. It is very important to follow the vaccination instructions of the manufacturers.
For example, use of the live vaccine in breeding birds should at the latest be 6
weeks prior to pairing, as a shorter interval might lead to poor breeding
performance.
17
Chlamydophilosis (ornithosis)
 Different serovars of Chlamydophila psittaci (previously called Chlamydia

psittaci) can cause disease in a wide range of avian species. Serovar B affects
pigeons and doves, and serovar E can be found in pigeons.
 Disease in pigeons may be referred to as chlamydophilosis or ornithosis, and can
be associated with respiratory disease or diarrhoea,
 sometimes resulting in the death of severely affected birds.
 Disease can spread from pigeons to humans, causing 'flu-like signs, fever,
headaches, sometimes pneumonia, and very rarely meningitis and death.
Epidemiology:
a. Adult birds may appear to be healthy but can carry this organism, intermittently
excreting and passing it to other adults or young birds via the faeces, the
respiratory tract, through crop milk, and possibly into the egg.
b. Further multiplication occurs in the cells of the respiratory tract, digestive tract
and other organs such as liver, spleen and kidney.
c. The organism can survive in dried discharges for many months, leading to
significant environmental contamination.
d. Although disease can be caused by Chlamydophila alone, more commonly
ornithosis results from a combination of Chlamydophila plus other factors.
e. Respiratory disease could therefore be caused by a combination of

Chlamydophila and viruses (including paramyxovirus), bacteria, mycoplasmas
and trichomonads, or could be due to Chlamydophila plus the effects of a draught
to give the so-called 'one-eyed cold' (unilateral conjunctivitis commonly seen in
young pigeons).
f. Similarly, in recent years green diarrhea has been seen in young pigeons caused
by a combination of Chlamydophila plus circovirus or adenovirus infection,
contributing to 'young bird sickness'.
g. Increased excretion and the development of clinical disease may be precipitated

by various stress factors such as excessive training, racing or breeding,
overcrowding, inadequate or draughty ventilation, dampness in the loft, or poor
feeding.
18
Clinical signs:
a. All ages are susceptible, but clinical disease tends tobe worst in young birds.
b. In the respiratory form, affected birds may have conjunctivitis resulting in wet
eyes, swollen eyelids, periorbital loss of feathers and sometimes protrusion of the
third eyelid (Figure 7). Discoloration of the wattles due to a nasal discharge may
be apparent, and noisy breathing may develop, sometimes with open-mouthed
respiration.
c. If the organism damages the air sacs the birds may be reluctant to exercise or
have poor flying times.
d. If the digestive tract or kidneys are affected, birds drink excessively and have
green diarrhoea. In some birds a combination of respiratory signs and diarrhoea
may be seen.
Figure 7: Chlamydiosis
Diagnosis:
 A range of different post-mortem lesions may be present, including airsacculitls,
pericarditis, perihepatitis, enlargement of the liver and spleen, and watery green
intestinal contents. On other occasions, ornithosis may be present without
obvious signs being visible at post-mortem examination.
 The diagnosis of ornithosis can be difficult because the organisms are often not
detected in modified Ziehl Neelsen-stained smears from liver or spleen, but a
PCR for C. psittaci carried out on pooled viscera should confirm the diagnosis.
 The PCR can also be used to test faecal samples and conjunctival swabs collected
from live birds; because of the intermittent excretion of the organism in faeces, a
pooled sample of faeces collected on multiple occasions should be tested.
19
Treatment:
a. Doxycycline administered in the drinking water. An initial treatment period of 5
days is suggested by the product manufacturers, but this has to be extended.
b. In some countries enrofloxacin for 21 days is used to treat ornithosis in pigeons

with good success.
c. Other precipitating factors such as inadequate ventilation must also be addressed.
Control:
 The prevention of ornithosis in pigeons is not straightforward. Because C. psittaci
is widespread and because apparently healthy birds can be carriers, pigeons will
inevitably encounter the organism.
 Control measures must rely on keeping stress factors to a minimum, ensuring
good hygiene and ventilation in lofts and transporters, avoiding overcrowding,
and controlling other diseases such as trichomoniasis and paramyxovirus.
 Regular inspection of birds, with prompt treatment before the disease becomes
established, is also recommended.
Streptococcus gallolyticus infection:
Streptococcal septicaemia has been recognized in pigeons for several years and
the causal bacterium has been variously described as Streptococcus faecalis, S.
gallinarum, S. bovis and more recently S. gallolyticus.
Epidemiology
 S. gallolyticus has been isolated from the intestinal tract of around 40% of healthy
racing pigeons and the organism is almost certainly widespread in the
environment of pigeon lofts.
 Predisposing factors such as poor hygiene, overcrowding, damp loft conditions,
inadequate diet and concurrent disease are probably required before clinical
disease occurs.
 Several different strains of S. gallolyticus may be present in a loft, but the
significance of the different strains is unknown.
20
Clinical signs:
a. The disease may take the form of a bacteraemia or septicaemia, resulting in
damage to the liver or kidney, or may cause arthritis, tenosynovitis and myositis.
All ages can be affected, from young squabs to adult breeders.
b. In some cases deaths may appear to be sudden, in other instances death follows a
period of inappetence, weight loss and the production of slimy green faeces.
Lameness and inability to fly will be seen if the stifle, hock or shoulder joints or
pectoral muscles are affected, and palpation may detect swelling of the joints.
c. The condition in the UK is often sporadic, but a loft outbreak has been described
elsewhere in which a high percentage of adult female breeding pigeons could not
fly. Similar clinical signs have been seen after the experimental inoculation of
racing pigeons with S. gallolyticus, with additional histopathological evidence of
focal myocardial necrosis, meningitis and encephalitis.
d. Also can be cause respiratory problems in young birds.

e. Signs include a purulent discharge from the nostrils, pus in the choanal cleft, head
shaking and scratching at the nostrils with brown discolouration of the cere.
Sneezing can result in yellow pus on the loft wall. This is often described as the
'snots'.
Diagnosis:
 Post-mortem examination may reveal swelling and congestion of the liver, spleen
and kidney, purulent arthritis, and well circumscribed areas of pallor of the breast
muscles. The accumulation of gelatinous yellow fluid around the tendon of the
deep pectoral muscle has been described.
 The organism can be readily isolated using standard bacteriological techniques

from the viscera in cases of bacteraemia and septicaemia, but the recovery of the
organism from infected joints and muscles may be less successful.
 Demonstration of S. gallolyticus from the faeces or intestine only may not be

significant, because healthy birds can carry this organism in the digestive tract.
Treatment:
a. An antimicrobial sensitivity test should ideally be carried out on isolates prior to
treatment.
b. A good response to ampicillin In the drinking water has been described in

Belgium and amoxicillin is cunently licensed for use in racing pigeons in the UK,
administered in the drinking water for 3-5 days...
21
c. Additional factors in the loft that could have predisposed to disease must also be
remedied, otherwise further cases of streptococcosis could occur.
Control:
Hygiene measures, good loft management and the control of intercurrent diseases
should ensure that this organism only causes sporadic deaths in pigeon lofts.
E. coli (Collibacillosi(
Cause:
This disease, which is now though to be more prevalent in pigeons than once
suspected, is caused by gram negative bacteria's which can invade our lofts
through infected dust particles, rodent droppings, and trough infected pigeon
droppings coming into contact with eggs in the nest. Infected adult pigeons will
emit the bacteria throughout a pigeon loft .
Clinical signs:
a. Since the E. coli bacteria can manifest themselves in any part of the pigeon's
body, symptoms can be diverse.
b. Most often young will die in the nest, adult birds will become listless and lose
weight, and their droppings will become loose, mucous, and greenish-yellow in
appearance.
c. Sometimes the droppings will have a foul odor.
d. Occasionally some birds may have nasal discharges and respiratory problems
associated with this disease.
Treatment:
Doxycycline and other antibiotics administered in the drinking water. An initial
treatment period of 5 days
Prevention & Control:
a. Maintaining good loft hygiene and keeping rodents away from feed and water are
very important.
b. Also keeping dust and ammonia levels down will help to control any outbreaks.
22
c. General Antibiotics: Any fancier would be well advised to have a good general
antibiotic in his medicine chest. They can be useful as "first choice" drugs if and
when problems occur. General antibiotics are effective against a broad range of
both gram positive and negative bacteria.
d. But excessive use of them can really damage the microflora of the bird, therefore
most veterinarian suggest a use of Improver as it is called 'green antibiotic' and
will have the same effect that any anitbiotic, but will leave the good bacterias and
keep the balance of the pigeon intact.
Staphylococcal:
Transmission
 Transmission is by inhalation of infectious aerosols and ingestion of infectious
exudates.
 Mechanical damage to the beak and nostrils as a result of fighting in the loft or in
the race baskets also permits infection to occur.
Clinical Signs
a. Staphylococcal infections often cause respiratory problems in young birds
.
b. Signs include a purulent discharge from the nostrils, pus in the choanal cleft, head
shaking and scratching at the nostrils with brown discolouration of the cere.
Sneezing can result in yellow pus on the loft wall. This is often described as the
'snots'.
c. Staphylococcal infections may become established by extension of local lesions

or localisation of septicaemic conditions, and may be encountered as a
tenosynovitis or septic arthritis, usually of the hocks and feet (Figure 8).
Figure 8: Staphylococcal lesions on the toes ofa pigeon.
23
Diagnosis
Bacteriological culture from the choanal cleft will confirm the bacterial species
involved.
Treatment
a. Amoxycillin (890mg of 100% amoxycillin trihydrate powder per litre of drinking
water for five days).
b. Or tetracycline (lg of tetracycline hydrochloride 80% per 1.51itres of drinking
water for five days - equivalent to 60mg/kg) will aid in the control of infection.
Control:
 General loft management is particularly important.
 Attention must be given to ventilation, routine hygiene and overcrowding.
Pasteurella Multocida:
Transmission
Infection is spread by inhalation or ingestion of nasal discharges and faeces from
infected birds.
Clinical Signs:
a. P. multocida infection is an uncommon disease that can affect any age of bird.
b. Experimental infection failed to produce disease but did induce a carrier state.
c. Disease can occur following other predisposing stresses. Acute infection is
characterised by respiratory distress, watery discharges which may be seen from
the mouth, and mortality.
d. Chronic disease is characterised by respiratory sounds, purulent nasal discharges
and conjunctivitis with or without swollen sinuses. In addition there may be
nervous signs, arthritis and subcutaneous abscesses.
a. The lesions seen in the acute disease are those associated with a generalised
septicaemia with or without petechial haemorrhages.
b. Chronic infection is characterized by rhinitis, sinusitis, conjunctivitis, tracheitis
and pneumonia.
Diagnosis:
a. Rapid confirmation of the diagnosis can be obtained by making a Gram stain of
an impression smear from heart blood or the liver of the dead bird.
24
b. Cytological examination of smears from the nares and pharynx of birds with an
upper respiratory infection may reveal the typical bipolar staining Pasteurella-
like organisms.
c. Caution must be exercised in interpretation because these organisms can be found
in normal birds.
d. Additional routine bacteriological culture will also detect infection. It may be
necessary to incubate plates for 48 hours if negative after 24 hours.
Treatment:
Treatment of all the birds in the loft is advisable. Water soluble medication with
amoxycillin or tetracycline is preferable.
Control:
 It is important to try to detennine the source of infection, paying particular
attention to rodent infestation.
 Cats can be a problem, but they are usually actively discouraged from the 10ft.
 Infection may indicate a recent stress such as overcrowding, poor ventilation,
change in management or vaccination.
Other Bacteria:
Any pathogenic bacteria that cause a systemic illness can give rise to respiratory
signs. This includes Salmonella spp. and Erysipelothrix spp. infection, coli
septicaemia, yersiniosis, Staphylococcal, Streptococcal and tuberculosis. Avian
tuberculosis can cause disease in pigeons. It is uncommon in racing pigeons but
common in feral pigeons.
Mycoplasma:
 The incidence of mycoplasma in pigeon flocks is hard to assess. This is due

primarily to the difficulty in demonstrating the presence of the organism by
culture and serology. It is also due to its complication with other organisms (e.g.,
secondary bacterial invaders).
 The primary criterion for a diagnosis of mycoplasmosis in a pigeon flock is often
response to treatment.
 However, the drugs of choice for mycoplasma are also excellent chlamydiostatic
agents.
Host:
Three species of Mycoplasma have been isolated from both normal and sick
pigeons: M. columborale, M. columbinum and M. columbinasale.
25
Transmission:
 Infection is spread by inhalation and ingestion of contaminated respiratory or
faecal material.
 The incubation period is 7-14 days.
 The organism is shed in respiratory exudates and faeces. As with other
mycoplasmal infections, latency is common.
Clinical Signs & Treatment:
a. Symptoms that should lead the practitioner to suspect mycoplasma would include
sneezing, coughing, oculonasal discharge, and other general respiratory distress.
b. These more obvious signs of respiratory distress, however, may also be present in
chlamydiosis or bacterial and fungal infections in the respiratory system.
c. Sometimes the symptoms of mycoplasmosis in a flock may even be more

obscure.
d. Fanciers will often report no obvious illness in the adults or squabs of a flock but
a reduction in performance. For example, some birds may return days late after
training flights, may be reluctant to fly and return to the loft, and seem winded
earlier than the rest of the flock.
e. The presence of mycoplasmosis may be more evident in endurance breeds such

as racing homers, tipplers, high flyers, sky cutters, nose divers, rollers, and other
aerial acrobats.
f. Tylocine generally has been thought of as being the drug of choice for
mycoplasmosis, with lincomycin and erythromycin also considered to’be
effective. However, conversations with a European colleague suggest that many
strains of mycoplasma are resistant to these drugs.
g. Injections of individual patients at least once or twice daily is the preferred

treatment but is impractical in many flock situations due to the chronic nature of
the disease.
h. Tylan and erythromycin are very irritating to the musculature when injected, so
the potential damage to the career of a racer should be considered. Erythromycin
and spectinomycin are also often effective.
26
Chapter Three: Protozoa & Fungal diseases:
1. Protozoa diseases
a. Trichomoniasis (canker)
b. Spironucleus columbae (hexamitiasis(
c. Coccidiosis
d. Haemoproteus spp
2. Fungal diseases
a. Aspergillosis
b. Candidiasis
Trichomoniasis ('canker'):
 Trichomoniasis is caused by the flagellated protozoan Trichomonas gallinae. It is

a very common disease worldwide. The parasite can be found in approximately
80% of all pigeons examined. The infection is normally subclinical in adult birds
(carriers), but young or immunosuppressed pigeons are susceptible to clinical
signs.
 Some strains can cause a high mortality in pigeon populations. T. gallinae has a
direct life cycle and because it has no cyst form it is very sensitive to a dry
environment. Infection is normally via the oral route (drinking water, feed).
Transmission occurs from parent to offspring (via crop milk) or within transport
cabins when pigeons from different flocks use the same water.
Clinical signs and diagnosis:

a. Trichomonas infections normally affect the upper digestive tract (mouth,
pharynx, oesophagus, crop).
b. Clinical signs include lethargy, anorexia, ruffled feathers, regurgitation, dyspnoea

and sometimes diarrhoea.
c. During clinical examination, white to yellow plaques or caseous material can be

found in the mouth and the crop wall often is thickened (Figure 9).
d. A sweetish odour from the mouth is typical.
e. In young birds, the umbilicus and the liver can also be affected (Figure 10). These
alterations are normally diagnosed during necropsy.
f. Diagnosis is by taking a wet swab sample from the crop content. Although
staining is possible, the swab should be examined fresh to diagnose the parasites
by their motility. The organisms have four flagella and an undulating membrane.
A B
Figure 9: A- abscess in the crop. B- abscess in the oral cavity
27
A B
Figure 10: A- abscess of the umbilicus. B- multiple caseous abscesses in the liver
Treatment:
a. Treatment should include the whole flock since infestation can be caused by poor
hygiene and poor health control management.
b. Several drugs are available, such as metronidazole, ronidazole and carnidazole.
c. Treatment should include vitamin supplementation to increase general resistance

and, if necessary, treatment of accompanying or secondary infections.
d. Disinfectants are not absolutely necessary, since drying out of water containers
for approximately 48 hours is sufficient, but hygiene management should be
improved. A strict water hygiene routine is advisable, including a daily change of
water containers (they can be reused after 1 day of drying) and provision of a
sufficient number of containers.
e. Affected flocks should be rechecked after 2 weeks. Resistances to drugs have

been described. To reduce the risk of drug resistance, pigeons should be checked
regularly for parasites and treated only on positive findings.
f. Unnecessary treatments may also weaken the bird and may reduce racing
performance.
28
Spironucleus columbae (hexamitiasis):

 The causative agent of hexamitiasis is Spironucleus columbae (formerly
Hexamita columbae, It can cause severe diarrhoea in young pigeons. Adult birds
play a role as asymptomatic carriers.
 Infestation with clinical signs is normally the result of a combination of poor
hygiene and accompanying bacterial, viral or parasitic infections.
 The parasite lives in the duodenum and small intestine and is spread by the
faeces. Spironucleus lacks a cyst form and is therefore very sensitive to a dry
environment.

a. Clinical signs are diarrhoea of varying extent, with greenish loose to watery
faeces, general depression, dehydration and weight loss.
b. Sometimes undigested seeds are seen in the faeces. Vomiting is also possible.
c. Mortality in young pigeons is up to 80%, depending on immune status and
secondary infections. Spironucleus columbae can be demonstrated in fresh warm
wet faecal samples.
d. The organisms are identified by their motility (rapid darting motion, in contrast to
the jerky motions of trichomonads).
Treatment:
Therapy includes vitamin supplementation and hygiene control. Metronidazole
and ronidazole can be used.
Coccidiosis:
a. To a small extent coccidians can be found in most pigeons and are not considered
to be harmful.
b. There is ongoing debate on whether or not coccidia should be treated if found
only in low numbers without clinical signs.
c. Undoubtedly small numbers of the protozoan will Induce immunity, but the
racing season is stressful for the bird and a few coccidians might become a large
problem within a few days, resulting in a loss of racing performance.
d. Therefore, treatment is advisable in racing pigeons during the season, though in
young pigeons or breeders there is induction of immunity and no treatment
should be considered. In contrast, high concentrations of the organism can
negatively affect performance and also cause severe clinical signs.Under crowded
conditions and poor hygiene, coccidiosis can become a problem for the whole
loft.
29
e. Two species are common in pigeons: Eimeria columbae and E. labbeana. They
have a direct life cycle with a faecal-oral infection route.
f. They live and reproduce within the mucosa in the intestinal tract. They replicate
in the host cells and can cause severe damage to the mucosa. Young pigeons are
more susceptible to clinical signs.
g. Development of clinical signs might depend on variations of the pathogenicity.
h. The oocysts that are shed with the faeces are very resistant in the environment
and can survive for more than a year.

a. Clinical signs develop rapidly (4-7 days) after ingestion of a relatively large
number of sporulated oocysts.
b. Moderate to severe diarrhoea can occur, with watery, dark or even bloody faeces.
c. Depression, anorexia, lethargy and emaciation can also be seen.
d. Diagnosis is based on the examination of the faeces in combination with the
results of the anamnesis and clinical signs.
e. Large numbers of oocysts normally can be found (flotation method), but the
number of oocysts seen has little relationship to the extent of the clinical signs.
f. The absence of oocysts does not exclude coccidiosis, since clinical signs can
develop faster than the shedding of the parasite (prepatence). Droppings should
be collected in the morning, since it has been reported that at this time of the day
oocyst concentrations are higher. It is also advisable to collect several samples.
Treatment:
a. Treatment should include all pigeons in the loft.
b. Vitamins (especially vitamins A and B) should be supplemented. Strict hygiene
and the use of disinfectants are essential.
c. Toltrazuril, sulphonamides or clazuril can be used to treat the flock.
d. After infection, a local immunity develops and normally prevents further clinical
signs, though reinfection is common.
e. There is no cross-immunity between different coccidian species, but the clinical
picture is normally mild after reinfection.
30
Haemoproteus spp:
 There are two species of Haemoproteus spp. that are known to infect pigeons and
doves: H. columbae and H. saccharovi.
 The former is spread by the pigeon louse fly (PseudoLynchis canariensis). The
incubation period is not known.
Clinical Signs:
This is generally a subclinical infection with any respiratory signs being
secondary to anaemia, emaciation and depression.
Diagnosis:
Confirmation is by identification of the parasite in the erythrocytes on a blood
smear.
Treatment:
Treatment is not usually necessary.
Control:
Control will involve controlling the vector.
31
Aspergillosis:
Aspergillosis is caused by fungi of the genus Aspergil- Lus, most commonly A.

fumigatus , but A. jlavus or A. glaucus may also be involved.
Transmission:
 Inhalation or ingestion of fungal spores, usually from environmental
contamination, bedding or feed.
 Incubation, Shedding and Latency This depends on tbe age of the bird, its
immunocompetence and the infective dose.
Clinical Signs:
a. There are no specific signs. However, infection is usua1ly chronic and there will
be loss of body condition.
b. The respiratory signs will depend on the site of the infection, but will include
dyspnoea, rattling sounds, rapid breathing, a fully open larynx, loss of condition
and dehydration.
c. Sometimes, infection occurs in the eye with swelling and the formation of a
yellow caseous plaque.
a. Diagnosis is most likely to be made on post-mortem examination.
b. Miliary white nodules in the lungs, syrinx, bronchioles and air sacs are typical of
a mycotic infection.
c. Compression of the lung expresses white strands of pus from the cut surface.
Wrute plaques of mature fungal growth with dark green to black centres may be
found on the air sacs.
d. In cases of acute AspergiLLus spp. pneumonia there may be no plaques.
Diagnosis:
The combination of clinical signs, post-mortem lesions and microscopical
examination of smears for fungal hyphae or spores will confirm the diagnosis.
Differential Diagnosis:
Acute salmonellosis, trichomoniasis, pigeon pox, 'oneeyed cold'.
Treatment
There is no satisfactory treatment.
32
Candidiasis
Candidiasis is a mycotic disease that is normally caused by Candida albicans and
might affect young pigeons.
Clinical Signs & Treatment:
a. Since yeasts can be found regularly in pigeon faeces, treatment is only necessary
in birds with clinical signs (e.g. voluminous faeces, yeasty odour from the mouth
or the faeces, thickened crop wall).
b. Candida infections should always be considered to be a secondary problem, and

underlying diseases should be diagnosed.
c. Treatment is possible using nystatin (orally to individuals, 100,000 lU/kg over 10

days). For treatment of the flock, chlorhexidine added to the drinking water (2.5
ppm) can help to resolve clinical signs, but is not a specific treatment.
33
Chapter Four: Parasitic diseases:
1. Worm infections
a. Helminths
b. Roundworms
c. Hairworms (threadworms(
d. Stomach worms
e. Tapeworms
f. Strongylids
2. Ectoparasites
a. Fleas
b. Mosquitoes
c. Lice
d. Parasitic Mites
Worm infections:
The most common worms found in pigeons today are roundworms hair worms,
stomach wall worms, gapeworms, stromglylids and tapeworms .
General Symptoms:
 The symptoms vary with the type of infestation, and conceivably pigeons can live
with slight infestations and show no ill effects. Severe infestations generally
cause droopiness, loss of weight and some diarrhea.
 Gapeworms can cause breathing problems. The best way to determine if a worm
problem exists is to have the droppings checked.
Helminths:
 Worms are among the most frequent contributors to ill health in domestic pigeons
and doves.
 Whether a primary cause of illness or a stress allowing the bird to be less
immunocompetent and subject to more severe illness with other pathogenic
organisms, they must be controlled to maintain optimum health. The incidence of
infestation and type of worms involved vary geographically with climatic
conditions.
 The presence of insect vectors is important in promoting or limiting infection.
Eggs can usually be easily demonstrated by flotation with sodium nitrate,
although direct smears sometimes reveal ova that are not as often found on floats
(e.g., Tetmmeres sp).
 Effective treatments are available for helminth parasites; however, identification
is necessary because some wormers are quite effective against some worms and
not for others. No single anthelmintic is the drug of choice for every type of
worm.
Roundworms:
 Roundworms are probably the most common although least devastating of the
worms found in domestic pigeons. Ascaridia columbae are more likely to affect
young birds than yearlings and old birds.
 Female roundworms produce large numbers of eggs, which larvate in the
environment and hatch in the intestine of the new host after ingestion.
 The larvation and prepatent period is affected by temperature and humidity but is
probably about 1.5 to 2 months.
34
 Weight loss, unthriftiness, and poor performance may be the symptoms of

infection, but many birds may be asymptomatic (especially those with light worm
burdens).
Hairworms (threadworms):
 Capillaria are quite common and often quite debilitating parasites of pigeons.
 Eggs are passed in the feces, larvate in 1 week or slightly longer, and are picked
up from the contaminated environment directly by the new host.
 The females begin to produce eggs and further contaminate the environment in 2
to 4 weeks.
 Even lightly infested birds may show symptoms of anorexia or at least decreased
appetite with subsequent weight loss. Heavy infestations may result in severe
illness or death due to emaciation, dehydration, and anemia.
 Postmortem findings may reveal an irritated small intestine and the presence of
the small, 0.5-inch, very thin worms.
 Follow-up flotations are beneficial to ascertain effective treatment. However,
eggs may be shed up to 3 to 5 days after elective treatment due to the eggs being
caught in the intestinal villi.
Stomach worms:
 Tetrameres americana and Diaspharynx nasuta infect the proventriculus.
 They suck blood, which causes anemia, and irritate the stomach wall, which often
causes severe digestive upsets.
 An intermediate host is required for both species, and infection occurs after
ingestion of the infected insect (roach, sowbug, beetle).
 The prepatent period for Tetrameres is about 1.5 months and closer to 1 month
for Diaspharynx.
 Tetrameres are more common in the southern United States. A thickened
proventriculus, blisters, and the large female Tetrameres may be found on
postmortem examination.
Tapeworms:
 Rallietina sp. and Aporina (Taenia) delafondi are the most common tapeworms
of pigeons.
 An intermediate host is required, and even the feather louse has been suspected.
Symptoms are often obscure.
 Unthriftiness, watery or mucoid droppings, weakness, and leg paralysis have been
reported.
35
 Diagnosis is made by observing the proglottids in the feces or demonstrating the

worm in the lumen of the small intestine on necropsy.
Strongylids:
 Ornithostrongylus quadriradiatus is not often seen, but is occasionally reported.
 The life cycle under optimum conditions may be completed in 1 to 2 weeks.
 Mildly infected birds may show no signs of illness. Ruffled feathers, weakness,
and excessive thirst may be seen in more severe cases.
 Vomiting, intestinal irritation, and hemorrhage may precede death in the worst
cases.
Treatment:
 Before considering which anthelmintic to use for which parasite, the veterinarian
must realize that reinfection is likely to occur unless rigid sanitation practices are
performed on contaminated environments.
 Removal of infected feces and elimination of intermediate hosts are necessary.
 Periodic fecal examinations should be done to recognize reinfection or new
infections before they escalate to disease-causing levels.
 Levamisol (13.65% solution) dosed at 1000 to 1500 mg/gal drinking water is very
effective for roundworms, is effective for capillaria (although some reports
conflict), and is not effective for stomach worms and tapeworms. Ten milliliters
of the injectable (1365 mg) in moderate temperatures is a convenient way to
worm a flock. Vomiting may occur in hot weather or in breeding flocks with too
much water intake, but this rarely causes problems. Individual treatment can be
accomplished at 20 mg/lb body weight (for a bird the size of an average racing
homer), with the injectable given orally or one tablet of Spartakon (Janssen
Labs). Levamisol can be quite toxic and should not be injected, especially at these
recommended dosages.
 Mebendazole (Telmintic; Pitman-Moore, Washington's Crossing, NJ) is a fairly

safe wormer that is effective against most worms except tapeworms. It is used for
flock worming at 0.5 teaspoon/gal drinking water for 3 to 5 days. Individual bird
treatment may be accomplished by administering 5 mg/kg once daily for 5 to 7
days.
 Fenbendazole (Panacure; Hoechst-Roussel Pharmaceuticals; Somerville, NJ) at

10 mg/kg once daily for 3 days has been shown to be 99% effective in removing
roundworms and hairworms. At 3 mg/kg once daily for 3 to 5 days it has been
shown to be 94% effective. Adverse reactions have been rarely and sporadically
reported and include feather abnormalities when used in molting birds. This drug
is seldom used by the author.
36
 Ivermectin (Ivomec or Equalan; Merck & Co., Rahway, NJ) is very effective
against stomach worms and capillaria. It is moderately effective against
roundworms. It is not effective against tapeworms. The author's recommended
dose is 0.5 to 1 mg/kg as an individual bird treatment. No adverse effects have
been noted, even at higher dosages. Tapeworms are treated with praziquantel
(Droncit; Miles) at 10 mg/kg injectable or 0.25 cat tablet by mouth for a bird the
size of an average racing homer.
Ectoparasites:
Fleas
 Two species of fleas are of particular significance, the European chick flea
(Ceratophyllus gallinae) and the stickfast flea (Echidnophaga gallinacae The
pigeon fly is probably the most dangerous parasite that can attack birds.
 It lives most of its life on birds, leaving only to lay its eggs somewhere in the loft.
Pigeon flies bite the birds often, and besides causing considerable discomfort,
they can be a major cause of pigeon malaria .
Mosquitoes:
 Mosquitoes would have to be considered the next worst parasite, simply because
they are found in almost all climates.
 They are the most common carrier of the pigeon pox virus .
Lice:
 Two species of lice are commonly found on pigeons, the slender louse
(Columbicola columbae) and the large body louse (Menapon latum). The slender
louse may be seen particularly between the barbules of the feathers when held
against the light.
 The eggs are laid in the groove between the feather shafts and the barbs. The
body louse lays its eggs in a similar situation and causes damage (appearing as
pin pricks) to the barbs of the feathers.
Parasitic Mites:
37
 Several species of mites live on the outside of the feather. They can be observed
resting like beads along the hafts of feathers and they can give rise to a good deal
of irritation and feather damage.
 The depluming mite (Cnemidocoptes lae vis lae vis) is the cause of feather rot. It
inhabits the skin at the base of the quill. The feather follicle and the feathers
frequently break off leaving a shortened stub, perhaps 2-3mm in length,
projecting from the skin. Bald areas occur and. whilst the appearance is
characteristic, it can be misleading.
 The pigeon quill mite (Syringophilus columbae) is less common but causes
similar damage. It inhabits the inside of the feather shaft and is therefore difficult
to see. However, under a microscope, particularly at x50 magnification under a
stereo microscope. they can present a spectactular sight (dodgem C,U"S in three
dimensions!). Their habitat makes them inaccessible to routine treatment.
 The scaly leg mite (Cnemidocoptes mutalls) is not primarily a pigeon parasite. but
it can cause evere crusty lesions of the legs and feet as a result of burrowing in
the scales. It must be differentiated from pox, bumblefoot and gout.
 The red mite (Dermanyssus gal/inae) is a very destructive ectoparasite with a

broad avian host range. Much of the life cycle is spent away from the host, but
populations may build up explosively, particularly in the summer months, and
blood sucking can lead to severe anaemia and even death of the host. Parasites
may not be pre ent on the bird when presented for examination a they only feed at
night. but the anaemic state of the bird and the unclean appearance of the skin is
suggestive. On post-mortem examination, ingested, engorged mites may be found
within the oesophagus and crop. The mites roost underneath furniture within the
loft, ego nest bowls, or in crevices in the structure.
 The Northern fowl mite (Ornithonyssus sylviarum) is a rather similar parasite,

though a larger proportion of its life cycle is spent on the body of the bird. These
are relatively large mites which can be seen, certainly in their adult form, with the
naked eye and which, when engorged. are bright red.
Diagnosis:
 Ectoparasites are numerous and common. It is satisfying to observe these with the
naked eye but identification is complex. Ectoparasites may be cleared on a
microscope slide in I % sodium hydroxide. Several specimens may be needed
(mounted on one slide) to observe all of the diagnostic characteristics. The
presence of an ectoparasite alone does not establish the existence of skin disease.
38
 Birds presented wi.th a deplumed area, probably littered with broken feather
stubs, are a particular problem. Detailed examination frequently fails to
demonstrate ectoparasites or any other specific causes. Diagnostic techniques
which have proved of assistance are the digestion of feather stubs and feathers
immediately surrounding the stubs overnight in 1% sodium hydroxide at 37°C (a
V-bottomed container such as a 30ml universal or a centrifuge tube is suitable for
this purpose). Microscopic examination of the deposit should reveal ectoparasites
or their parts clearly against a background of amorphous material.
 Sealing of feathers and stubs under suspicion in a small closed plastic envelope
for at least 24 hours is often useful. Parasites tend to migrate from such material
and become caught in the folds of the envelope. With a microscope they may be
found readily under low power magnification by direct examination through the
plastic.
 Examination of the undersides of furniture in the loft must be carried out

carefully if dermacid mites are to be incriminated.
 The microscopic examination of suspicious encrustations leared with I % sodium

hydroxide is potentially useful , but in many cases such examinations prove
negative, particularly when extensive earlier treatments have been attempted.
Treatment:
 Mites and lice may be treated by routine use of dusting powders. (NB. The use of
chlorinated hydrocarbon compounds is contraindicated in the treatment of birds.)
 In general, mite infestations can be treated with cypemlethrin 0.5% as a spray or

dip.
 Burrowing mites in particular may be treated with ivermectin (I % solution

diluted 1:9 with sterile water immediately prior to use - give 0.2mllkg i/m).
 Application of the same dose directly onto the skin over the back may also be
effective. (NB. Solutions of ivermectin in water are unstable and must be
prepared immediately before use. Stock solutions may be prepared in propylene
glycol [beware of wet bottles]).
39
Chapter Five:
1. Nutritional disease
a. Vitamin deficiencies and toxicosis:
i. Vitamin B deficiency
ii. Vitamin D deficiency
b. Mineral/electrolyte deficiency or overdosage
i. Calcium and phosphorus
ii. Sodium, potassium and chloride
iii. Magnesium
iv. Iodine
2. Malnutrition and loss of performance
3. Intoxication with feed or medication
4. Mineral toxicosis
5. Drug overdosage
6. Poisoning:
a. Mycotoxins
b. Organophosphates
c. Insecticides
Nutritional disease
Vitamin deficiencies and toxicosis:

 A long-lasting complete absence of a particular vitamin in the diet can lead to
avitaminosis. Because of modern husbandry conditions, with only restricted free
flying or even complete housing in aviaries, the birds no longer have any access
to natural vitamin sources.
 The vitamin content of diets based on grain is generally not sufficient to meet the
bird's demands, especially as its content varies depending on the quality of the
grains and method of storage.
 Furthermore, demand is increased during the breeding, racing and moulting
periods and so deficiencies may be observed more often. Therefore pigeons
require vitamin supplementation during these periods of high demand in
particular.
Vitamin B deficiency:
 In pigeons only vitamin C can be synthesized endogenously. Vitamin K and the B
vitamins can be obtained from intestinal flora, but B vitamins, as major promoters
of metabolism, should still be supplemented during the racing season. Food-
additive manufacturers offer a broad selection of vitamin preparations to satisfy
all vitamin needs.
 From experience, the administration of B vitamins exhibits the greatest effect
when given at the end of the week, i.e. the last two days before the day of the
race. It is important to ensure that all compounds are of high quality and are
stored under adequate conditions, as B vitamins in particular are extremely
sensitive to high temperatures.
 An inadequate supply of B vitamins is followed by a general decrease of the
bird's metabolic capacity and thus decrerased vitality. This leads to unsatisfactory
breeding, moulting and racing results.
 The classic disease resulting from vitamin B deficiency is known in pigeons. It is

characterized by a dysfunction of the nervous system; the birds show
opisthotonos and are unable to stand (Figure 11). If this stage is reached, birds
usually die.
 The disease is caused by sole feeding of predominantly unpeeled grains. This is

now hardly ever seen, since modern commercial feed mixtures contain vitamin
enhanced extruded or coated corns. Prophylaxis is most important.
40
Figure 11: Signs of vitamin B1 deficiency. (© Michael Lierz)
Vitamin D deficiency:
 Lipid-soluble vitamins are closely related to crucial functions in the pigeon's
metabolism. Vitamin D functions as a regulator for calcium-phosphorus
homeostasis and is of major Importance during the breeding period, as it directly
Influences egg shell quality and the skeletal development of young birds.
 Even if the mineral supply is optimal, skeletal malformation can occur if vitamin
D is deficient. Vitamin D precursors are found in germ buds and converted to the
active form through the influence of ultraviolet light, which is why access to
natural sunlight is vital. Nevertheless, vitamin D should be supplemented during
the breeding season to avoid diseases such as rickets.
 This disease particularly occurs in undersupplied nestlings. The typical signs are
growth retardation, a misshapen sternum and poor feathering in young birds.
 Adult birds lacking vitamin D can show paralysis during laying, since the bird's
calcium demand exceeds the amount that can be absorbed from the intestine.
 Consequently calcium is mobilized from endogenous storage In the bones. In

most cases this disease is not simply vitamin D deficiency but a consequence of
inadequate mineral supply and insufficient access to sunlight.
 Vitamin D dosages must always be measured out accurately, since lipid-soluble

vitamins are stored in the body and oversupply can lead to irreversible damage,
e.g. calcification.
41
Mineral/electrolyte deficiency or overdosage
For undisturbed metabolism, reproduction, growth, moulting and high racing

performance an adequate supply of minerals and electrolytes is essential. Otherwise
decreased performance ability and an enhanced susceptibility towards diseases will
occur. Major elements/ electrolytes are required in higher doses and include calcium,
phosphorus, potassium and chloride, of which calcium is the most important. Of the
trace elements, iodine is of highest significance.
Calcium and phosphorus

 Calcium is involved in bone development, cell metabolism, muscle activity,
blood coagulation and egg shell production. Since the calcium content of grain
mixtures is usually not sufficient, pigeons must be provided every day with grit
mixtures, which generally contain calcium-rich clamshells. Calcium deficiency
during the reproductive period results in a reduced quality of the egg shell (which
is about 90% calcium carbonate).
 It may also lead to paralysis in laying birds as a consequence of the mobilization
of huge amounts of calcium from endogenous storage for egg shell production. In
young pigeons, calcium deficiency leads to 'rickets' (see also vitamin D
deficiency, above) of which a typical sign is a deformed sternum. Adult pigeons
with calcium deficiency show osteomalacia.
 Phosphorus is abundant in legumes and cereal germ buds and therefore a

deficiency seldom occurs. In general, common mineral and grit mixtures contain
calcium and phosphorus in the optimal ratio of 2:1. Regular ad libitum supply
with such feed additives on a daily basis is important, but it is also important that
excessive dietary phytates do not bind calcium, thus reducing its bioavailability.
Sodium, potassium and chloride

 Sodium, potassium and chloride are responsible for the maintenance of the cell's
osmotic pressure and are also required for absorption and transportation of
nutrients.
 Furthermore they are involved in the conduction of electric potentials from cell to
cell. Sodium and chloride are usually sufficient in feed mixtures. Higher contents
can be found in mineral and grit mixtures, in which salt (NaCI) is often used to
make the mixtures more attractive for the pigeon.
42
 Mixtures with a high salt content are usually ingested eagerly, but the breeder
should only offer them in a restricted manner, to avoid sodium poisoning or
dehydration.
Magnesium
 Magnesium is vital for conducting electric potentials and for muscle activity.
During times of high performance there is an increase in demand for magnesium.
 Many electrolyte mixtures that are added to the normal diet after a race contain
magnesium to prevent deficiency signs.
Iodine
 Both during the growth period and for high performance metabolism during
racing, an adequate supply of iodine is essential. Iodine-containing preparations
are included in nearly every nutritional concept for pigeon breeding as well as
racing to increase the pigeon's performance.
 These preparations have a clear positive effect on the pigeon's general condition.
Iodine has several other important functions. Iodine is contained in higher
amounts in grit mixtures, especially if they contain clamshells.
 During periods of high performance the additional supplementation of such

preparations may well be required. With iodine deficiency, hyperplasia of the
thyroid gland will occur.
 This has been documented in pigeons several times but no longer plays a major
role today, thanks to the general provision of high-quality feed.
 Provision of this trace element is by regular feeding of iodine-containing mineral
mixtures. Therapy involves administration of commercially available iodine-
containing drugs over several weeks.
Malnutrition and loss of performance

 Modern feeding techniques and an increasing professionalism in the sport of
pigeon racing have helped to make the occurrence of classic nutritional diseases
such as those described above a rare event.
 During the breeding season there are sporadic cases showing clinical signs
resulting from the undersupply of certain nutrients, but in many cases this is more
often the result of poor health status and consequently inadequate utilization of
nutrients than a true undersupply. High demands are made on pigeons concerning
their physical fitness. The birds can only meet these demands if they have been
properly supplied with all essential nutrients from the egg. The basis for high
performance during the racing season (which is the most important time for the
breeder) is the optimal provision of nutrients at all times of the year. All too
43
frequently breeders only worry about their pigeons' health status just as the racing
season is about to start.
 At this point it is too late to compensate for neglect during the rest of the year. As
explained above, special commercial feeds with a protein content matched to the
demands of the breeding period, the moult and the racing season, along with a
generous supply of minerals and the regular administration of vitamins
(especially lipid-soluble vitamins), are required. Nutritional deficits are likely to
express themselves in poor feathering during breeding and moulting.
 Dry and rough feathers with poor pigmentation and socalled 'fret marks'
(translucent lines in the feather) indicate undersupply or poor utilization of
nutrients. Deficits can also be apparent in growth retardation and general poor
development of the bird. Well-developed birds have dense and smooth feathering
that is rich in pigmentation, whereas undernourished birds
 are skinny and badly feathered.
 Successful pigeon racing depends on many factors. Quality of the bird, health
status and the environment of the housing are key points. Optimal nutritional
provision during the racing season is an additional factor and this is where many
breeders make elementary mistakes. Breeders offer homemade pigeon feeds and
mix feed additives to compile their own provision plan that is often mismatched
with the actual demands of the pigeon. The result of inadequate nutrition during
times of high stress will be exhaustion, which in the majority of the cases can be
seen from midway through the racing season. Malnutrition also decreases the
pigeon's defence system against infection.
 Therefore a well-balanced diet and short periods of recreation between the flights
are crucial. Since with increasing flight distances the demand for essential
nutrients also rises, the bird's diet must be formulated accordingly.
Intoxication with feed or medication
 Severe intoxications associated with clinical signs have become rare in modem
husbandry, but there can still be huge differences in the quality of grain mixtures
and they might also be stored inadequately.
 This can lead to contamination of the feed and, depending on the kind of
contaminant involved, can result in clinical signs very similar to those for
toxicosis. Despite the high quality of commercial feed mixtures, there are still
occasional occurrences of feed pests such as various corn weevils and flour mites.
Feed mites, which grow optimally in feed that is stored in warm damp conditions,
44
can lead to digestive problems in the pigeon if ingested, and also promote
secondary growth of mould fungi.
Mineral toxicosis
 The administration of mineral supplements can also cause signs of intoxication.
Especially during the rearing season, young pigeons develop a real hunger for
salts to match their high demand.
 Mineral and grit mixtures and 'pigeon stones' are often picked up eagerly. In cases
where the sodium chloride content of these feed additives is too high, intoxication
expresses itself in watery to mucoid faeces.
 With severe NaCI intoxication massive withdrawal of water leads to the death of
the bird.
 A short withdrawal of ad libitum feeding of the mineral mixture is helpful and
mineral drinks or less attractive mixtures should be given instead.
Drug overdosage
 Intoxications can be associated with the application of drugs via drinking water or
feed. In most cases this is because the breeder has used the wrong dosage. Low
dosages in the range of few grams cannot be measured precisely with measuring
spoons. Also most pigeon breeders are well provided with all the very common
drugs and often use them without due care. Another factor of vital importance is
the amount of water uptake, since this varies depending on the ambient
temperature. As a general rule for the administration of drugs via drinking water,
it is assumed that the intake of drinking water is 1 litre/day for 20 pigeons. If the
ambient temperature is very high, this intake can easily double. This would lead
to an increased intake of the drug if the dosage remains the same.
 The problem is often seen with nitroimidazole. a drug that is commonly used for
the treatment of trichomoniasis. Young pigeons in particular are extremely
sensitive to overdosage and develop clinical signs such as torticollis, resembling a
paramyxovirus infection. Clinical signs mostly disappear when the administration
of nitroimidazole is stopped.
 Another common sign of intoxication is a problem with moulting, which may be

caused by the administration of sulphonamides and antiparasitic drugs (e.g.
fenbendazole). The administration of fenbendazole is very difficult, due to the
need for exact dosing; overdosage leads to severe liver and kidney failure that
results in the death of the bird.
45
 There have been instances of overdosage of streptomycin, which causes

reversible paralysis but may also lead to death.
Poisoning
 In general terms, the treatment of toxicoses in members of the Columbiformes is

similar to the treatment in other birds or mammals: remove the bird from the
source of the toxin, eliminate the toxin from the bird's body, administer a specific
antidote if possible and give supportive treatment.
 The avian respiratory anatomy makes it a much more efficient gas exchange
system than that of the mammal and thus they are much more sensitive to inhaled
toxicoses, including inhalation of mycotoxins in poorly maintained lofts.
Fortunately, because most pigeons and doves are kept in extensive systems, they
are less likely to be affected by domestic inhaled toxins (e.g. from overheated
non-stick utensils) and will not be exposed to household plants and food items;
also, being granivorous, they are unlikely to ingest significant amounts of lead
unless metal particles or shot have been dropped or scattered in grit that the birds
may be picking up.
 Because of their plumage, pigeons are less prone to cutaneous absorption of

toxins than mammals, but they may ingest toxins from their feathers during
preening or may even inhale particulate toxins from the plumage when sleeping.
The lifestyle of the free-flying pigeon puts it at greater risk of being exposed to
agricultural pesticides, herbicides and rodenticides. The majority of pigeons are
reasonably selective feeders and will reject any grain that appears 'spoiled'.
However, pigeons feeding in fields and picking at moss and debris in gutters are
at the greatest risk,
 Spoiled food items are more likely to be found In aviaries containing the more
exotic varieties of doves and pigeons that also live on fruit.
 The risk from owner-administered drug treatments is quite high. Because fanciers
will dose their birds with everything that is on the market, toxicoses are often a
flock rather than an individual event. Depending upon the toxin, signs of
poisoning include incoordination, seizures, respiratory distress, weakness,
diarrhoea, polyuria or sudden death. They must be differentiated from infectious
disease with similar signs.
46
Mycotoxins:
 Mycotoxins are produced as chemical metabolites by some fungi. The conditions

for the production of mycotoxins may be very specific for a particular fungus.
Unfortunately, they are undetectable by sight, smell or taste. Mycotoxins may be
present with no visible signs of mould (fungus) growth.
 The amount of toxin produced may vary and is also variable within different parts
of a batch of food. There are many mycotoxins. The clinically significant ones for
the pigeon are ochratoxin, deoxynivalenol (vomitoxin) and the tricothenes.
Contact dermatitis is a possibility with the tricothenes.
Clinical signs
 These relate to hepatoxicity, prolonged clotting times, kidney dysfunction and
depressed immune system function.
 Depression, haemorrhages, anorexia, polyuria, erosive lesions of the oral mucosa,
constriction of digits, immunosuppression and neurological disorders can all be
seen.
Diagnosis
 Diagnosis of mycotoxicosis in the live bird is difficult since clinical signs are
non-specific and vague or because they mimic other diseases.
 Diagnosis is based on the finding of mycotoxins in the food or the gastrointestinal
tract.
 Unfortunately, the food may not be available for testing, since it may all have
been ingested, consumed some time previously or eaten whilst away from the
pigeon loft. Culturing the fungi and identifying mycotoxins can be a lengthy
process.
 Tricothenes (Fusarium spp.): necrotic lesions from ulceration of the orophharynx

and gastrointestinal tract.
 Ochratoxin (Pencilllum and Aspergillus spp.): non-specific and often secondary

infections present due to immune system depression and secondary infections
(e.g. air sacculitis). It is both hepatotoxic and nephrotoxic.
 There is no specific treatment and the history of a change in food may be a
diagnostic indicator. It is essential that a new food source is given to the birds if
mycotoxicosis is suspected.
Post-mortem examination:
 Some fungal toxins cause hepatic cell degeneration and bile duct necrosis.
 An enlarged pale liver and enlargement of the spleen and pancreas is thus seen on
post-mortem examination.
47
 Gastrointestinal haemorrhage from altered clotting ability is common.
Insecticides
 The risk from residual pesticides applied to foodstuffs is unknown.
 Pyrethrins (often combined with piperonyl butoxide) have the lowest toxicity for
birds when applied topically.
 They can be toxic if applied at high concentrations or following inhalation.
Clinical signs
Clinical signs include weakness, anorexia, central nervous system signs,
dyspnoea and death.
Organophosphates:
 Signs of OP poisoning are related to inhibition of acetylcholinesterase and may
vary with the age of the bird and the degree of exposure, with chronic exposure
possibly resulting in poor hatchability.
 Delayed toxicosis can occur 7-10 days after exposure to OPs. These signs are due
to an organophosphorus ester-induced neuropathy rather than inhibition of
acetylcholine activity.
Diagnosis
 History of possible exposure to insecticides and clinical signs form the basis for
diagnosis.
 Assay of cholinesterase levels in plasma (to measure depression of
cholinesterase) and also in tissue at post-mortem examination (especially brain)
may confirm organophosphate and carbamate toxicity.
 However, 'normal' values for pigeons may be difficult to find. Post-mortem
diagnosis from gastrointestinal contents or tissues is possible.
Treatment
For acute OP toxicosis, atropine and pralidoxime chloride (2-PAM) are
administered, or atropine alone for carbamate poisoning.
48
Type Signs Diagnosis Treatment

Iatrogenic toxicoses
Ivermectin Seizures, blindness, History of Fluids, warmth, supportive
death administration therapy
Dimetridazole Tremors, ataxia, History. Excessive Fluids

weakness, seizures consumption of
medicated water fed
to nestlings
Levamisole Vomiting, ataxia, Vomiting is Nursing

catatonia, dyspnea immediate clinical
and death sign
Fenbendazole Feather History of injectable Nursing and fluids
abnormalities. doses > 70 mg/g
Vomiting,
neurological signs
and death
Quinolones
Dyspnoea, muscle
tremors
Aminoglycosides Nephrotoxicity or Blockade High doses Fluids and supportive
neuromuscular given to dehydrated treatment
birds
Herbicides, rodenticides and agricultural poisons
Organophosphates Weakness, muscle Contaminated water Atropine every 4 hours;
and carbamates tremors, ataxia, sources, pralidoxime
(chlorpyrifos, diazinon, seizures, paralysis, insecticides and chloride: wash affected
carbaryl, malathion, death in young birds fertilizers. feathers:
dichlorvos) Cholinesterase in activated charcoal, fluids,
plasma and brain diazepam and
nursing
Alpha-chloralose Coma or death 2.5% causes Warmth and

(avicide) anaesthesia and anticonvulsants
hypothermia; > 2.5%
is lethal
Coumanns: warfarintype Depression, anorexia, Vitamin K

petechiation,
epistaxis
Coumarins: second Similar signs More toxic, more difficult to

generation treat
Metaldehyde Fits, ataxia, coma Slug bait Flush crop; anticonvulsants;

keep in
darkness
49
Fungal toxins
Vanous (e.g. Depression, anorexia, Eaten mouldy grain Symptomatic nursing
ochratoxin, vomiting, or food
tricothenes. vomitoxin. ergot) polyuria, Diagnosis can be
haemorrhage, very difficult - find
paralysis, etc. toxin in food or Gl
tract contents
Plant poisoning
Laburnum {Laburnum Fitting, vomiting, Time of year and Empty crop of seeds; fluids
anagyroides) and Broom ataxia, dyspnoea, exposure to seed and
(Cytisus spp.) death pods symptomatic therapy
Other potential toxicoses

Sodium chloride Polydipsia/polyuria History of exposure Usually returns to normal in
to excessive 12 hours.
intake of salt IV fluids if hypovolaemic
Heat Vomiting, Inadequate Cold bathing: immerse bird

Incoordination, ventilation in pigeon in cold water
ataxia and basket; shut in
death vehicle in hot
weather
Table 2: Toxicoses: clinical signs, diagnosis and treatment
50
Chapter Six: Other diseases:
1. One-Eyed Cold
2. Sour Crop
3. Haemochromatosis
4. Visceral gout
5. Articular gout
One-Eyed Cold
This syndrome can be a result of one or more of the following infections: pigeon
herpesvirus, chlamydiosis, mycoplasmal infection, trichomoniasis and bacterial
infections.
Clinical Signs
 One-eyed cold is a common infection found primarily in younger birds. It tends
to affect individuals over an extended period of time.
 Usually, only one eye is affected. Initially, there may be swelling of the eyelids
with closure of the eye, excessive lacrimation, staining of the feathers about the
eye and discolouration of the cere.
 This can progress to keratoconjunctivitis and permanent blindness if treatment is
not instituted quickly.
Diagnosis
 Diagnosis is on clinical signs alone.
 The bird should be screened for trichomonads.
Differential Diagnosis
Pigeon herpesvirus and pigeon pox.
Treatment
 An antibiotic ophthalmic ointment should be applied to the eye for at least seven
days (chlortetracycline ointment should be used to control possible Chlamydia
spp. infection).
 Affected birds should be treated with doxycycline (one 20mg tablet per bird for
five days).
 The slow spread of this infection makes individual bird treatment preferable to
flock medication. If trichomoniasis is suspected, all the birds in the in the
appropriate section of the loft should be treated.
Sour Crop
 The most common problem associated with the crop is so-called 'sour crop'. The
crop becomes thickened, and distended with fermenting impacted food. There is a
fetid odour. Affected birds lose condition and their droppings may be loose.
 Diagnosis presents no problems, but the condition itself may be complicated by

trichomoniasis, candidiasis, capillariasis or bacterial infection .
51
 Stained smears from crop samples should be examined microscopically for

pathogens. The contents of the crop should be gently massaged out or, if this is
impossible, removed surgically .
 The bird should be maintained on a minimum quantity of a light diet whilst

recovery occurs. Fluid therapy, including electrolytes, and also antibiotics may be
helpful. The traditional use of bicarbonate of soda solution to wash out the crop is
contraindicated due to potential renal damage.
Haemochromatosis
 Haemochromatosis is not a common condition in pigeons but occurs where there
is excessive accumulation of iron causing pathological changes in the liver and
other major organs.
 The condition arises from an altered intestinal absorption of iron, possibly from
an inherited defect, and also from high dietary iron content (sometimes by
excessive iron supplementation by the fancier).
Clinical signs
 Clinical signs relate to the physical changes in the liver, namely hepatic
enlargement, ascites and swollen abdomen.
 Fluid accumulation by pressure on air sacs can lead to weakness and respiratory
signs (e.g. coughing). Sudden death without previous signs occurs.
Diagnosis
 Definitive diagnosis is by liver biopsy and use of Perle's iron stain. Plasma
biochemistry may show an increase in AST levels and a decreased level of
plasma proteins.
 Radiography may reveal hepatomegaly, ascites and sometimes cardiomegaly.
 Ascitic fluid is a yellowish transudate.
 Blood iron levels are not diagnostic.
Treatment
 Ascitic fluid should be removed if the bird is dyspnoeic, but not too much fluid
should be removed at one time since the procedure may induce shock.
Phlebotomy is useful and 1-2% of the bird's blood volume can be removed daily
until either there is a clinical improvement or the haematocrit reaches the lower
end of the range for the species (PCV not lower than 30%.
52
 Thereafter, weekly phlebotomy may need to be carried out at volumes of about

1% of body weight. Serum albumin should also be monitored.
 Deferoxamine has been used to reduce the level of iron in body tissues. The bird
needs to be on a lowiron diet and should not be given supplemental iron by the
fancier.
 Other parenchymal hepatic conditions can be diagnosed by liver biopsy.
Visceral gout
Visceral gout occurs when uric acid crystals (as white flecks) are deposited on the
serosal surface of the liver and other organs (e.g. kidneys and pericardium), death
following soon after. It is often a post-mortem diagnosis.
It may follow an episode of severe dehydration or nephritis and Is an acute and serious
disease with a poor prognosis. Tubular secretion of uric acid stops, anuria or oliguria is
seen and plasma uric acid levels rise rapidly.
Signs of gout are non-specific and may include weight loss, anorexia and emaciation.
Sudden death is common and may relate to cardiac embarrassment from the pericardial
and epicardial urates or hyperkalaemia.
Diagnosis
Plasma uric acid levels are usually elevated (though if the uric acid crystals are
deposited on the serosa, the plasma level can decrease and might be within normal
range) but these are not diagnostic since other conditions can also cause raised uric acid
levels.
Laparoscopy is the single most useful investigative procedure, but many cases will only
be diagnosed at post-mortem examination.
Treatment
In the acutely ill bird intensive supportive therapy (especially fluids) and allopurinol
administration may, in some cases, reduce the plasma levels of uric acid but will have
no effect upon the previously deposited urates. (Allopurinol reduces the production of
uric acid from purines and is unlikely to be of great benefit in cases with nephron or
ureteral obstruction.)
53
Articular gout:
In articular gout, uric acid crystals are laid down in and around joints and in tendon
sheaths. Once uric acid deposits have occurred they can 'grow', forming larger
accumulations of uric acid called tophi.
Deposition occurs when the plasma uric acid level is slightly above the solubility of
sodium urate in the plasma. It is an extremely painful condition for the bird, resulting in
lameness or drooping of the wings.
Diagnostic techniques include aspiration of tophi: needle-shaped uric acid crystals are
seen under the microscope. A murexide test involves adding one drop of nitric acid to
the material on a slide and heating until dry, then adding one drop of ammonia. A
mauve colour indicates the presence of urates.
Treatment of renal disease

Supportive therapy with fluids, heat and nutritional support should be given until a
specific diagnosis Is reached. Parenteral fluids may be indicated in the most severe
cases.
In anuric or oliguric pigeons, the fluid should initially be restricted to the daily
insensible fluid loss of 20 ml/kg and diuretics (furosemide) given. Monitoring body
weight accurately will give an indication of over- or under-hydration.
The hydration status of polyuric pigeons must be monitored and fluid given as needed.
Antibiotics should be administered since there is a higher susceptibility to renal invasion
from portal vein-carried enteric organisms. Antibiotics that are potentially nephrotoxic
should not be used but multivitamin support should be given. Allopurinol or colchicine
can be considered in the most severe cases but long-term use may cause renal damage.
A more detailed description of renal diseases, diagnoses and treatment can be found in
Lierz (2003).
54
Chapter Seven: Breeding & Racing:
1. Normal breeding
2. Diseases associated with Breeding:
a. Infertility
b. Embryonic mortality
c. Contamination
3. Racing season
4. Resting period
Normal breeding
 To understand some of the potential problems, it is important to know the normal
breeding cycle. Pigeons lay clutches of two white eggs. Breeding would occur all
year round if the environmental conditions were suitable. The fact that the
majority do not is a direct result of interference by the fancier separating the
sexes. However, so called 'late breds' is a common feature of the sport. These are
the young from pairs of birds that have either tlown particularly well during the
season or are from paJ1icuiarly valuable stock birds. They will generally have
been bred to sell.
 The breeding season begins with the pairing of the hen and cock birds. This can
occur any time after the moult has been completed, ie. December.
 The timing of pairing will depend on the requirements of the fancier and his
method of racing, ie. Natural system or the widowhood system. The new year's
ring numbers are available from January I st. Only young birds bred that year can
be entered for young bird races. Consequently, if the aim is to have the best
developed and trained birds for the young bird races (July to September), the
closer they are hatched to January 1st the better. This would be the case ifadults
are tlown on the widowhood system (old bird races are from mid-April to the end
of July). Pairing would be later (March onwards) if the birds are tlown on the
natural system.
 One section of the loft will contain the nestboxes. The number will depend on the
size of the section. Each nestbox will contain a nest bowl, pots for feed and water,
and moveable partitions that allow the birds to be confined. The cocks will be
introduced and allowed to pick their own nestbox. The fancier will have decided
on the pairings and the hen will then be introduced to the cock bird.
 The first egg will be laid in the evening about 10 days later. The second egg is
laid about one and a half days later in the early afternoon. Incubation commences
when the second egg has been laid. Both the cock and the hen take it in turns to
incubate the eggs. Candling the egg will reveal infertile eggs. After five days of
incubation the blood vessels of the chorioallantoic membrane can be seen. By 10
days the egg will have become opaque as the embryo ha, grown. At this time the
only feature discernible will
 be the air cell. The first egg will hatch after 18 days and the second egg up to a
day later. It may take J 5-20 hours for the squab to hatch from the first moment
that it is seen to have pipped the eggshell.
 The squab i fed predominately on crop milk by the cock and the hen bird for the
first seven days of its
 life. This milk is produced by the cells lining the crop. The changes to the crop
begin at about the sixth day of incubation. The crop reache its greatest thickness
55
by the fifteenth day of incubation, continuing until the squab is seven days of age
(re ting crop weighs 1.7g; an actively secreting crop weighs 15g). The crop milk
consists of 8.6% fat. 12.4% protein, 1.4% minerals and 77.6% water. There is no
carbohydrate in crop milk. When the squabs are about four day of age the crop
milk wi ll begin to contain some partially digested feed. From about seven days
of age the squab will be fed predominately on regurgitated feed. The squab
weighs about 14g on hatching, and it will then rapidly gain weight. By the fourth
day it will weigh 63g and at 20 days it will weigh 400g (nearly the adult
bodyweight). During this time the juvenile feathers will have developed. The
squab is normally weaned at about 24 days of age when the feathering has fully
developed.
Diseases associated with Breeding

 The first indications of breeding problems will be failure of the bird to lay or the
layi ng of only one egg; failure to detect embryo development if candling is
practised; failure of the eggs to hatch; or early squab mortality. Broadly, the
problems can be classified as follows:
 Infertility - failure to lay eggs or fai lure of embryonic development.

 Contamination - evidence of bacterial or fungal contamination of the egg.
 Embryo mortality - early and late embryonic mortality will be the commonest
findings .
 Neonatal mortality - the squabs will fail to thrive or suddenly stop thriving. Dead
or moribund squabs should be examined.
 The type of problem being experienced can be determined initially by examining

eggs and chicks. Unfortunately, many fanciers will present the offending pair of
adu lts without appreciating that they have just disposed of the most useful
evidence.
 The deficiency diseases described result from experimental work with poultry,
but they should be expected to cause similar problems in pigeons.
Infertility
 No eggs or too many eggs. Same sex – sexing pigeons is done on body
conformation, hence this could be a problem for the inexperienced fancier. A
salpingitis could have resulted from an earlier generalized infection or be the
result of stress, ego inappropriate vaccination of hens between pairing and laying.
 The bird may be too young or too old.
 Too many feathers around the vent. This can interfere with mating. The feathers
around the vent should be trimmed.
56
 Too much disturbance. This may be the re ult of overcrowding, cracked eggs
through constant movement on the nest, fighting for nestboxes and throwing of
eggs out of the nest bowls by intruders into the nestbox. This could also result in
ectopic eggs.
 Failure to mate. Copulation should have oCCUlTed 24-48 hours before the egg is
laid in order to ensure fertilisation.
 Too high a temperature. ie. 30°C, will result in lower fertility. However, too cold
a temperature, ie. 4°C. coupled with damp, is more likely to be a problem,
particularly for matings that occur very early in the year. Increasing day length is
also an important stimulus for reproduction. The provision of extra artif iciallight
may be required.
 Both underweight and overweight birds will have reduced fertility. Attention to
the diet and regular checks of body condition will avoid this problem. An ample
source of fresh water must be avai lable. The fat hen is more likely to develop
abdominal hernias, retain the egg or suffer from prolapse of the cloaca or oviduct.
 Deficiencie. Vitamin A - decreased sperm counts, reduced sperm motility,
increased numbers of abnormal sperms, irregular laying cycles. Vitamin B6
(pyridoxine) - poor egg laying. Vitamin 0 1 - (thin shells and soft shells) and
irregular laying cycles. Vitamin E - testicular degeneration if low levels fed for a
prolonged period.
 Nervous disorders. This could result from overzealous use of dimetridazole,
pigeon paramyxovirus infection, salmonellosis or cypermethrin dips. The cause
must be diagnosed and treated accordingly.
 Infection of the reproductive tract. This could be the result of generalised
infection or secondary to a stress in the case of salpingitis.
 Congenital and inherited diseases. Accurate breeding records should indicate if
this is likely to be a problem.
 Hormone imbalance, ego tumours of the ovary or testes.
 Overbreeding. This could lead to inertia of the oviduct and calcium deficiency.
This is most likely to be seen in a hen that is on her second or third round of eggs.
She may have laid the first egg but not the second. The presenting signs are
sudden onset of nervous symptoms and an inability to walk. Fly or feed. The
author has found that crop tube feeding with Rapidaid (Vetrepharm) (lOg/I OOg
bodyweight in two doses over 24 hours) and calcium tablets (0.25 of a 300mg
tablet once daily) gives a rapid improvement in this condition. The second egg is
then laid. The eggs are discarded. It is several weeks before the hen fully regains
normal f1ight.
 Therapeutics. Sulphonamides are known to predispose to thin shells and poor
hatchability. Mebendazole is contraindicated in breeding birds. Ointments that
adhere to the vent feathers may be transferred onto the shell. thus blocking the
pores and reducing hatchability.
57
 Eggshell damage. Calcium deficiency in the diet can predispose to thin shells and
membrane eggs. The former will permit the hairline cracks and toe holes to be
made more easily.
Possible cause Comments

Lack of condition Poor husbandry or diet, nol in breeding
condition, under-exercised, poor weather
conditions, vitamin deficiency
Age Older birds or very young birds
Subclinical disease PMV, bacterial (especially Salmonella),
chlamydial, protozoal
Endo/ectoparasites
Drugs Anthelmintics and antibiotics, especially
fenbendazole and sulphonamides
Physical factors Too fat. tumours, oviductal abnormalities,
hormonal imbalances. Pairing two males or
females
Lack of fertilization (clear eggs) Cloacal obstruction with faeces or feathers.
Infertile cock bird. Incompatibility, arthritis,
hormonal problems, pairing of two females
Damaged eggs Trauma from nails. Thin-shelled eggs

Thin-shelled Calcium and vitamin D deficiencies (lack of
sunlight); intercurrent disease
Deformed eggs Inherited predisposition, salpingitis
Double yolks Twin embryos can live almost until the point of
hatching
No yolk present Ovarian dysfunction or blockage ol proximal
oviduct
Dead-in-shell Bacterial infection of egg (e.g. Salmonella or E.
coli); absorption of chemicals through shell;
lack of oxygenation
(e.g. egg pores blocked - use straw instead of
sawdust); genetic abnormalities. Eggs cracked -
clumsy birds or
disturbances when sitting (e.g. irritation from
red mite infestation), chilled eggs, nutritional
deficiencies, lott
humidity too low, temperature too high (lethal if
overheated)
Inability to hatch Humidity too high during incubation or too low
at hatching; wrong positioning within egg. Weak
chicks – nutritional Problems.
Table 3: Causes of Infertility.
58
Contamination
Poor nestbox hygiene. loft hygiene and inappropriate nesting materials will
predispose to contamination of the eggs. Fresh straw and tobacco stalks are often
provided as nesting materials. Hay should not be given because it will rapidly go
mouldy and the long strands can wrap themselves around the legs of the squabs.
These problems are always worse if there are concurrent shell quality problems.
Microbiological examination will identify the causal agents, ego bacterial
(Escherichia coli, Pseudomonas spp. Salmonella spp.) or fungal (Aspergif/us
spp.).
Embryonic mortality
Early
 Parents not incubating eggs (see Excessive Disturbance).
 Chilling - very cold weather and parents not sitting for long periods.
 Vitamin A deficiency - loss of epithelial membrane structure, hence failure to
develop blood vessels and reduced hatchability.
 Biotin deficiency - two peaks of mortality at the beginning and end of incubation.
(For lesions see Late Mortality.)
 Vitamin E deficiency - oedema, death.
Mid-term
 Parents not incubating eggs.
 Thin shells and egg drying out.
 Vitamin BI2 deficiency - malposition, oedema, curly toes, poor muscling.
 Vitamin B2 (riboflavin) deficiency - stunted chicks with oedema.
Late
 Parents disturbed during incubation.
 Insufficient humidity because of lack of water for parents.
 SaLmonella typhimurium infection either in the oviduct or through the eggshell
resulting in death.
 Deficiencies.
 Inbreeding can result in more malpositioned embryos being found.
 Malposition.
59
Deficiency Comments
Vitamin B 6 Poor hatchability.
Vitamin D3 Stunted chicks, soft bones, chondrodystrophy,
poor hatchability.
Vitamin E Poor hatchability.
Pantothenic acid Subcutaneous haemorrhages and oedema. The
age of mortality depends on the severity of the
disease.
Biotin and folic acid (folacin) Micromelia, syndactylism, bradygnathism, death
occurring after pipping of the air cell.
Vitamin K Haemorrhage and death of the embryo.
Phosphorus Soft beaks and legs, poor hatchability.
Calcium Poor hatchability, short thick legs, short wings,
short lower mandible, pliable beak and legs,
oedema of the neck, bulging forehead,
protruding
Zinc Skeletal abnormalities. Wings and legs absent.
Manganese Short wings and legs, abnormal head, parrot
beak, retarded growth, oedema.
Selenium Poor hatchability, oedema.
Table 4: Effect of various deficiencies on late embryonic mortality
Racing season
 During the racing season a systematic feeding programme is the basis for
successful results. The performance demands on the racing pigeon every week
are extremely high and demand-based feeding
 is especially vital in this period. Since pigeons usually undergo one race every
week with a 7-day interval, there is a special feeding programme for the days
between flights.
 Directly after the race, electrolytes and high-quality and highly digestible energy
sources, such as glucose, are given in order to shorten the period of time for
recovery. The diet on the day of return and the first
 few days thereafter should also include a high amount of carbohydrates and fat,
but at the same time be highly digestible through lower protein content. At the
beginning of the week the diet should consist of a higher fibre fraction, which
accelerates the purging of the intestine.
 During the phase of recovery and reconstruction of lost body tissues in the middle
of the week, the protein content of the diet must be elevated. Towards the end of
the week the diet should be high in fat to restore the pigeon's energy sources.
Modern feed mixtures contain very low protein concentrations, resulting from the
almost complete absence of legumes. It is common for food additives containing
highly digestible proteins and amino acids to be added to the normal diet to
satisfy the need for these substances.
60
 Since the pigeon gains most of its energy supply during the race from burning
fats, seeds with high fat contents are included in high proportions in modern feed
mixtures. Moreover, several compounds containing different kinds of oils for the
provision of extra energy are also added. The demands for vitamins (especially
B), minerals and trace elements are equally increased during this phase and many
food additives are available to counterbalance possible deficiencies. Feedstuff
and food-additive manufacturers offer complete packages for total care during the
racing season. As well as specialized feed mixtures and food additives, these also
include preparations to support the bird's metabolism in order to increase the
racing pigeon's fitness level in general.
Resting period
 During the resting period in winter, an adequate diet is comparably low in protein
content and fibre and the energy content must not be too high. The goal for this
period of comparatively low exercise is to avoid overfeeding and excessive
weight gain.
 However, if the ambient temperature is very low the energy level of the diet must
be increased, e.g. by adding extra maize. There are various commercial products
available. It is important not to switch to a different type of feed too abruptly.
 Approximately 3 weeks before the start of the breeding season the diet for the
resting period should steadily be replaced by the breeding diet.
61
References:
Beynon, P.H., Forbes, N.A., Harcourt-Brown, N.H. (1996). Manual of raptors, pigeons
and waterfowl. BSAVA Publishing, Gloucester, UK.
Brugère-Picoux J., Vaillancourt J.P., Shivaprasad H.L., Venne D. and Bouzouaia M.

(2015). Manual of Poultry Diseases. Association Française pour l' Avancement des
Sciences, Paris.
Chitty J., & Lierz M., eds. (2008). BSAVA Manual of Raptors, Pigeons and Passerine
birds. BSAVA Publishing, Gloucester, UK.
Rosskopf, w. J. And r. W. Woerpel. (1996). Diseases of cage and aviary birds, 3rd
Edition, Williams and Wikins, Baltimore, Maryland.

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Manual of Pigeons Diseases

‫د‪ .‬ﻋﻠﻲ ﻛﺮﯾﻢ‬

Section No. Content Page No.

3 Pigeon adenovirus infection

Section No. Chapter Two: Bacterial Diseases Page No.

Section No. Chapter Three: Protozoa & Fungal Page No.

3 Spironucleus columbae (hexamitiasis(

Section No. Chapter Four: Parasitic diseases Page No.

Section No. Chapter Five Page No.

2 Vitamin deficiencies and toxicosis: 40

6 Calcium and phosphorus

Section No. Chapter seven: Breeding & Racing Page No.

2 2. Diseases associated with Breeding

Section No. References 62

Chapter one: Viral Disease:

2. Pigeon circovirus infection

3. Pigeon adenovirus infection

4. Necrotizing hepatitis (adenovirus type II(

5. Pigeon herpes virus infection

Figure 2: Paramyxovirosis (PMV1). Balance disorder.

Pigeon circovirus infection

Clinical signs ('young bird sickness')

a. There is no specific treatment for circovirus infection, and it must instead be

Pigeon adenovirus infection

 Inclusion body hepatitis associated with an adenovirus infection became a

b. Post-mortem examination is often unspectacular, but there may be a catarrhal

c. Evidence of concurrent infections such as crop candidiasis, trichomoniasis and

f. Attempts to isolate pigeon adenovirus are frequently unsuccessful, therefore

Treatment and control:

Necrotizing hepatitis (adenovirus type II):

a. A necrotizing hepatitis of racing pigeons associated with an adenovirus infection

Pigeon herpesvirus infection:

Figure3: Pigeon herpesvirus: necrotic debris in the

d. Histopathological examination of the liver typically demonstrates foci of

c. Painting the lesions with aqueous iodine may be beneficial.

d. Antibiotics to control secondary infection may also be necessary to ensure that

Chapter Two: Bacterial Diseases

3. Streptococcus gallolyticus infection

b. Losses of appetite, green diarrhea (Figure 6) and increased mortality or

c. Weight loss can be rapid and severe.

e. A small proportion of the birds may develop abnormalities of the central

fibrosis. Bacteriology, including selective cultures for Salmonella, should be

c. This could be followed by a course of probiotics in the drinking water.

e. Following treatment and loft disinfection, pooled faecal samples should be

 Different serovars of Chlamydophila psittaci (previously called Chlamydia

e. Respiratory disease could therefore be caused by a combination of

g. Increased excretion and the development of clinical disease may be precipitated

b. In some countries enrofloxacin for 21 days is used to treat ornithosis in pigeons

c. Other precipitating factors such as inadequate ventilation must also be addressed.

Streptococcus gallolyticus infection:

d. Also can be cause respiratory problems in young birds.

 The organism can be readily isolated using standard bacteriological techniques

 Demonstration of S. gallolyticus from the faeces or intestine only may not be

b. A good response to ampicillin In the drinking water has been described in

Prevention & Control:

c. Staphylococcal infections may become established by extension of local lesions

Figure 8: Staphylococcal lesions on the toes ofa pigeon.

 The incidence of mycoplasma in pigeon flocks is hard to assess. This is due

Clinical Signs & Treatment:

c. Sometimes the symptoms of mycoplasmosis in a flock may even be more

e. The presence of mycoplasmosis may be more evident in endurance breeds such

g. Injections of individual patients at least once or twice daily is the preferred

Chapter Three: Protozoa & Fungal diseases: