Pigeons (Columba livia domestica) belong to order Columbiformes and family Columbidae (Fig. 1). Pigeons are used in racing or pigeon sport, as ornamental birds, laboratory specimens, companion animals, and they are also raised for meat production. Free-ranging pigeons also thrive in many urban centers (Magnino et al 2009).
Below you will find a collection of differential diagnosis lists for common clinical problems observed in pigeons and doves. The clinical approach to the columbiform relies on the same concepts of “One Medicine” used in all species, however many of the infectious diseases listed are relatively unique to this taxonomic group, or at least much more prevalent when compared to psittacine birds or songbirds. These abbreviated rule-out lists should in no way replace professional judgment when evaluating your patient.
Diseases featured in the ‘Primer’
Taking the history
History of the columbid should include all the standard questions for the avian patient as well as vaccination history. Also determine:
- Is the bird considered a pet? A source of food? Or the member of a valued flock? This will determine if the owner’s focus is the health of the group or the individual bird.
- Does the pigeon (or owner) have exposure to wild pigeons, pigeons in other lofts, or bird shows?
Non-specific signs of illness
Non-specific signs of illness can include anorexia, weight loss, lethargy, a fluffed and ruffled appearance, and poor general condition. The pigeon fancier may report reluctance to fly or poor racing performance (Table 1).
|Table 1. Important differential diagnoses for the pigeon with non-specific signs of illness (De Herdt and Pasmans 2009, Silvanose 2008, Zwart 2008, Coles 2007, Hooimeijer 2006, Rupiper 1998, Hooimeijer and Dorrestein 1997)|
|Bacterial disease||Salmonellosis (paratyphoid)||Commonly results in a chronic carrier state
Source of infection is feral pigeons
|Streptococcus gallolyticus||Facultative pathogen
Septicemia most common between January to August*
|Chlamydophila psittaci||Chlamydia is usually part of the ornithosis complex of pigeons, however disease can also be associated with weight loss, fluffed plumage, polydipsia, and diarrhea in birds.|
|Mycobacterium avium subsp. columbae||Chronic emaciation, ruffled feathers, and/or slow molting|
|Viral disease||Circovirus||Lethargy, weight loss, and poor performance are typical presentations in young birds.|
|Paramyxovirus-1||Can cause polyuria/polydipsia with no other clinical signs|
|Poxvirus||Affected birds often exhibit anorexia, weight loss, and staining of the feathers on the neck or "hackle".|
|Parasitic disease||Trichomonas||Associated with poor racing performance in adult pigeons|
|Hexamita||Wasting may be the only clinical sign observed.|
|Fungal disease||Candidiasis (thrush)||Inadequate growth, ruffled feathers, inappetence, and weight loss|
|Metabolic disease||Heat stress|
|Toxic exposure||Heavy metals|
|*Based on observations in Belgium (De Herdt and Pasmans 2009)|
|Paramyxovirus-1 (PMV-1) is a variant of the mesogenic strain of Newcastle disease virus (NDV) that affects pigeons and doves. Paramyxovirus-1 first originated in the Middle East in the 1980s, but is now found worldwide (Bonfante et al 2012, Coles 2007, Rupiper 1998). Paramyxovirus-1 is a reportable disease in the United Kingdom and Australia (NSW 2015, Coles 2007). It is important to recognize that infection with PMV-1 is very different in pigeons than in chickens and other avian species, and pigeons appear to be more resistant to NDV infection (Greenacre 2005).
Paramyxovirus can be ingested or inhaled and is transmitted by direct contact with infected pigeons or fomites. Clinical disease is common in pigeons that have not been vaccinated, particularly wild pigeons (Coles 2007). All ages are affected, however young birds are most at risk. In western Europe, PMV-1 infection typically occurs during the late summer and fall (De Herdt and Pasmans 2009).
Clinical signs of PMV-1 in pigeons can resemble NDV except that little or no respiratory disease is observed. The clinical picture can include (De Herdt and Pasmans 2009, Coles 2007):
Diagnosis can be confirmed with paired or multiple serologic titers or viral isolation. Common histologic findings include nonsuppurative infiltrate in the pancreas, kidney, and brain (De Herdt and Pasmans 2009, Coles 2007). Treatment relies on supportive care until the bird is able to maintain hydration and eat on its own (Harlin and Wade 2009).
Annual vaccination using inactivated adjuvanted vaccine (AviPro 111 PMV-1, Lohmann Animal Health International; Nobilis, Novibac; Colombovac PMV, Pfizer) significantly lowers the risk of clinical disease and should be pursued 1-2 months prior to the breeding season or 6-8 weeks before racing or showing. Birds can be vaccinated from the age of 3-4 weeks and should be boostered annually. Expedient vaccination, including in young birds, in the face of an outbreak is recommended (Harlin and Wade 2009). When vaccinated pigeons develop clinical disease, European legislation requires that all pigeons in close contact with affected birds be euthanized (De Herdt and Pasmans 2009, Hooimeijer 2006).
Common diseases of young birds
There are a variety of infectious diseases commonly seen in squabs, squeakers, and young birds (Table 2).
|Table 2. Common diseases of young pigeons (Harlin 2013, Raidal 2012, De Herdt and Pasmans 2009, Coles 2007, Greenacre 2005, Hooimeijer 2006, Rupiper 1998, Hooimeijer and Dorrestein 1997)|
|Bacterial disease||Colibacillosis||Although this facultative pathogen can cause disease in nestlings, “young pigeon diarrhea” caused by overgrowth of E. coli typically occurs in young pigeons after their first training flight.|
|Salmonellosis (paratyphoid)||Retarded growth rate, death
Sudden and virulent outbreaks can occur; the source of infection is feral pigeons.
|Chlamydophila psittaci||Usually a part of the ornithosis complex in pigeons, C. psittaci is also an important cause of diarrhea, polydipsia, fluffed feathers, respiratory disease, ocular disease, and weight loss in young birds.|
|Viral disease||Circovirus||Lethargy, weight loss, respiratory distress, diarrhea, and poor performance in birds between 1 and 4 months of age.|
|Herpesvirus||Acute death, diphtheritic inflammation of the larynx, esophagus, and trachea
Minor role in coryza
|Adenovirus type I||Non-specific signs of illness, polyuria/polydipsia, watery green diarrhea, vomiting, weight loss in pigeons < 1 year of age.
|Poxvirus||Hypertrophic proliferation of the epithelium, predominantly around the beak and on the eyelids.|
|Parasitic disease||Trichomonas||Sudden death and wasting are common presentations.|
|Hexamita||Most commonly observed during spring and summer months|
|Ectoparasites||Dermanyssus gallinae and Ornithonyssus sylviarum are blood-sucking mites. Argas reflexus is a blood sucking tick. These ectoparasites can cause death in nestlings.|
|Fungal disease||Candidiasis||Inadequate growth, ruffled feathers, inappetence, regurgitation, and weight loss|
|Trauma||Cannibalism||Overcrowding, other stressors|
|First described in pigeons in California, USA in 1990, pigeon circovirus (PiCV) is now found worldwide (Raidal 2012, Hooimeijer 2006).
Although the method of transmission is unknown, PiCV is frequently diagnosed in flocks that import new pigeons without use of proper quarantine protocols. Birds less than 4 months of age are particularly susceptible; most infections in weaned birds and adults follow a subclinical course. There are no seasonal or sex predilections.
The clinical picture can include (Harlin and Wade 2009, Schmidt et al 2008, Hooimeijer 2006):
• Non-specific signs of illness such as lethargy, weight loss, and poor performance
• Respiratory distress
• Death in 3 to 5 days
Circovirus infection can be part of young pigeon disease syndrome, a multifactorial syndrome that appears to be particularly common in central Europe. The syndrome is associated with multiple secondary infections presumably due to immunosuppression caused by PiCV. Stressors, such as overcrowding and inclement weather, are considered a predisposing factor (Raidal 2012, Schmidt et al 2008).
Histopathologic evaluation of the bursa of Fabricius, thymus, liver, kidney, brain, crop, intestines, and spleen will reveal intranuclear inclusions. Diagnosis can be confirmed via electron microscopy or PCR (Raidal 2012, Coles 2007, Hooimeijer 2006).
Management of PiCV in the individual bird relies upon supportive care and immune modulators such as interleukin. Disease is prevented by quarantine, stress reduction, and careful attention to sanitation.
|Pigeon herpesvirus or PHV-1 is shed in feces and oropharyngeal secretions. Clinical disease predominates in squabs from uninfected parents, and systemic disease is most commonly seen between 2 weeks and 10 weeks of age. Herpesvirus is transmitted to the young from latent infections in other birds. Infection is usually asymptomatic in adult birds, although some immunosuppressed individuals will exhibit mild signs for 1 to 2 weeks. Latent infections persist for life. Historically, more than 50% of racing pigeons possess antibodies against PHV-1 (De Herdt 2009).
The clinical picture can include (De Herdt 2009, Harlin 2009, Wernery 2008, Coles 2007):
• Anorexia, green droppings
• Mild upper respiratory signs (rhinitis, conjunctivitis)
• Diphtheritic plaques within the oropharynx, esophagus, and/or trachea, dyspnea
• Weakness, ataxia, wing tremors
• Sudden death in young birds
• Morbidity in up to 60% of affected birds
Diagnosis relies upon isolation of the agent from necrotic foci in the liver and spleen or the presence of intranuclear inclusion bodies within lesions (Cole 2007). The use of acyclovir at 80 mg/kg PO q 8 hours for 10 days can reduce mortality during an outbreak (Greenacre 2005).
Disease of the gastrointestinal tract
Oropharyngeal lesions are a frequent finding on physical examination of the ill columbid. Important differential diagnoses for caseous or diphtheritic lesions can include Trichomonas gallinae, poxvirus, herpesvirus, and candidiasis (De Herdt and Pasmans 2009, Coles 2007). Overgrowth of Candida albicans frequently occurs in overmedicated flocks. In addition to oropharyngeal lesions, birds with candidiasis can exhibit a crop distended with sour-smelling fluid, regurgitation, and anorexia. Tiny white or yellow nodules called sialoliths may also be identified on the palate. The cause and significance of this finding is unknown.
|Table 3. Important causes of vomiting or diarrhea in pigeons (De Herdt and Pasmans 2009, Harlin and Wade 2009, Silvanose, 2008, Zucca et al 2008, Zwart 2008, Coles 2007, Hooimeijer 2006, Rupiper 1998, Hooimeijer and Dorrestein 1997)|
|Bacterial disease||Colibacillosis||“Young pigeon diarrhea” occurs after the first training flight in 2 to 6 month old birds. Vomiting is also commonly observed with E. coli septicemia. Infection can also occur in adult pigeons.|
|Chlamydophila psittaci||Usually a part of the ornithosis complex in pigeons, C. psittaci is also an important cause of diarrhea and weight loss in birds.|
|Mycobacterium avium subsp. columbae||Chronic emaciation, diarrhea|
|Salmonellosis||Slimy green to yellow or bloody diarrhea. Commonly results in a chronic carrier state, however sudden & virulent outbreaks can occur. The source of infection is feral pigeons.|
|Viral disease||Adenovirus type I||Crop stasis, vomiting, weight loss, and/or watery diarrhea in young birds <1 year of age.|
|Circovirus||Diarrhea and weight loss in birds 1-4 months of age|
|Herpesvirus||Green droppings, infectious esophagitis (diphtheritic lesions within the oropharynx and esophagus), vomiting|
|Paramyxovirus-1||Watery or hemorrhagic diarrhea and vomiting or regurgitation|
|Parasitic disease||Capillaria||Capillaria obsignata and C. caudinflata are the most common nematodes reported in pigeons. Heavy infestations lead to vomiting, diarrhea, and weight loss.|
|Cestodes||Usually an incidental finding, however heavy infestations can cause diarrhea|
|Coccidia||Heavy infestations can cause enteritis, especially in young birds|
|Hexamitiasis||Heavy infestations can cause vomiting, diarrhea, polydipsia, weight loss, and dehydration. Feces are watery or mucoid, are intensely green and malodorous.|
|Trematodes||Hemorrhagic diarrhea can occur with heavy infestations. Very rarely seen in the US|
|Trichomoniasis||Diarrhea can be observed with heavy infestations as fluid droppings with a sour odor. Severe infestations can cause vomiting or regurgitation|
|Fungal disease||Candidiasis||Inadequate growth, ruffled feathers, inappetence, regurgitation, and weight loss|
|Toxic exposure||Organophosphates||Hypersalivation, vomiting or regurgitation, diarrhea|
|Heavy metals||Crop stasis, vomiting or regurgitation, diarrhea|
|Most pigeons and doves harbor the motile flagellate Trichomonas gallinae. Trichomoniasis or “canker“ is a very common infection in columbids. The organism is directly transmitted through saliva and crop milk, and squabs are typically infected during feedings. When offered as a feeder bird, columbiforms can also pass T. gallinae infection to falcons and hawks (De Herdt and Pasmans 2009, Stoute et al2009).
The clinical picture will vary with the virulence of the strain and the age of the pigeon. Most strains are low in virulence, and infected adults are often healthy carriers. Clinical disease tends to be more severe in juvenile birds. Trichomonas can be a primary pathogen or a cause of secondary disease in birds stressed by concurrent illness (De Herdt and Pasmans 2009, Stoute et al 2009, Coles 2007, Hooimeijer and Dorrestein 1997).
Trichomonas gallinae usually invades the mucosa of the oropharynx, esophagus, and crop. The initial lesions are quite small, but as disease advances the lesions coalesce to form white, caseous deposits with underlying necrotic ulceration. The infected crop wall will become thick and firm. Clinical signs typically include sensory depression, ruffled feathers, anorexia, weight loss, and regurgitation or vomiting. On occasion, trichomoniasis can extend into the proventriculus, conjunctiva, sinuses, beak, as well as the commissure of the beak or rictus. Heavily infected birds can exhibit a clear, mucoid oral discharge and oculonasal discharge, and they may even pass sour-smelling, watery droppings. In severe infections, lesions can also extend into the soft tissue of the head, neck, and orbit. Particularly virulent strains can descend the gastrointestinal tract in 1-3 week old squabs, eventually breaking through the intestinal wall and invading the large vessels and liver. This systemic form will spread to the liver, lung, mesentery, and heart (De Herdt and Pasmans 2009, Stoute et al 2009, Zucca and Delogu 2008, Coles 2007, Hooimeijer 2006, Charlton et al1991).
Diagnosis of trichomoniasis relies upon identification of the organism. Obtain a sample via crop lavage, crop swab with a moistened cotton-tipped applicator, or even suction of mucoid oropharyngeal discharge. Giemsa stain the slide (Fernando et al 2011, Coles 2007) or perform wet mount cytology by suspending the sample in a drop of warm saline solution or sterile water. Place the moistened sample on a slide or coverslip warmed to body temperature, and perform microscopic examination at low magnification (10X). The trichomonad organism is 5-19 µm in length with four anterior flagellae (De Herdt and Pasmans 2009, Stoute et al 2009).
Effective medical management involves 5-nitroimidazole derivatives including ronidazole, carnidazole (Spartix®, Wildlife Pharmaceuticals) (12.5-25 mg/kg PO once), dimetridazole, or metronidazole (25-50 mg/kg PO q12h x 5-10 days (Hawkins et al 2013, De Herdt and Pasmans 2009, Munoz et al 2008). Unfortunately pigeon fanciers often administer these medications prophylactically during the racing season, and acquired resistance to nitroimidazoles is possible (Munoz 1998, Franssen and Lumeij 1992). In the United States, these medications cannot be used in food-producing birds and management relies instead upon the reduction of stressors and culling severely affected birds (Stoute et al 2009).
|Hexamita columbae, also called Spironucleus columbae, is a flagellated parasite measuring 5-9 µm. Infection occurs by ingestion of infected cysts from droppings, food, or water. Clinical disease is most common with heavy infestations in young birds, up to 12 weeks of age. The clinical picture can include vomiting, watery or mucoid, intensely green and fetid diarrhea, polydipsia, weight loss, and poor general condition. Some young birds will acutely die during their first training period. Diagnose hexamitiasis via wet mount cytology of fresh cloacal swabs or via Giemsa staining. The organism can be recognized by its linear movement when seen microscopically, with optimal magnification being 200-400x. Like trichomoniasis, treatment relies upon 5-nitroimidazole derivatives. At necropsy, the crypts of Lieberkühn are filled with cysts and trophozoites. The parasite may also be seen on cytology of deep mucosal scrapings (De Herdt and Pasmans 2009, Coles 2007).|
|Eimeria labbeana and E. columbarum are common endoparasites of pigeons. Coccidiosis is diagnosed by microscopic examination of the feces. Low oocyst numbers do not require treatment, however shedding can be a non-specific sign of ill thrift and should not be ignored. Heavy infestations can cause diarrhea in nestlings. Treatment relies upon toltrazuril (Baycox®, Bayer) (20-35 mg/kg PO once or 20 mg/kg in drinking water x 2 days), clazuril, or sulfonamides. Minimize the risk of clinical disease with wire flooring, which prevents bird contact with contaminated feces, and regular cleaning of the loft to remove oocysts before they can sporulate (De Herdt and Pasmans 2009, Krautwald-Junghanns et al 2009, Vercruysse 1990).|
Coryza is a non-specific term for respiratory disease in pigeons. The underlying cause of disease is often multifactorial and can include infectious agents as well as non-infectious factors involving the loft (Box 1) (De Herdt and Pasmans 2009).
|Box 1. Loft factors that influence the incidence of respiratory disease in pigeons|
As in all avian patients, signs of early respiratory disease can be very subtle and the pigeon fancier may simply report poor racing performance or somewhat green, pasty droppings. As disease advances, the owner may observe epiphora, frequent swallowing, head shaking and scratching, and sneezing. Plumage over the shoulder or back may become wet from wiping the eyes and nares. Clinical signs will eventually include congestion, open-mouth breathing and dyspnea (Hooimeijer 2006).
On physical examination the normal cere should be dry with a collection of white powder down, but may instead appear gray and wet. There may also be evidence of conjunctivitis, dacrocystitis and/or pharyngitis. Yellow, diphtheritic membranes may be observed on mucous membranes of the oropharynx, tongue, and trachea (Hooimeijer 2006).
|Table 4. Important causes of respiratory signs in the pigeon (Duizer et al 2010, Dickx et al 2010, De Herdt and Pasmans 2009, Magnino et al 2009, Zwart 2008, Hooimeijer 2006, Vandamme 1998, Hooimeijer and Dorrestein 1997)|
|Bacterial disease||Ornithosis complex||Lethargy, weight loss, conjunctivitis, plugged nares, dyspnea|
|Viral disease||Herpesvirus||Mild conjunctivitis, rhinitis sometimes occur in young pigeons|
|Poxvirus||Wet pox can obstruct the trachea causing congestion and dyspnea|
|Circovirus||Respiratory distress can be seen in birds 1-4 months of age.|
|Parasitic disease||Trichomoniasis||Severe, virulent infection can cause nasal trichomoniasis in nestlings.|
|Metabolic disease||Heat stress|
|Trauma||Air sac compression|
|Toxic exposure||Toxic fumes|
Aspergillosis is seen only rarely and in individual pigeons. The incidence of disease may increase with environmental conditions that promote fungal spore production like straw bedding (Hooimeijer and Dorrestein 1997).
|Pigeons can contract mixed infections known as “ornithosis complex”. Potential pathogens include (De Herdt and Pasmans 2009, Hooimeijer 2006, Magnino et al 2009, Vandamme et al 1998):
Clinical disease is most obvious in young birds less than 12 months of age. Clinical signs can include lethargy, weight loss, conjunctivitis, keratitis, plugged nares, nasal exudate, sneezing, dyspnea, diarrhea, and polydipsia (Duizer et al 2010, Zwart 2008). Visit LafeberVet’s Avian Chlamydiosis for additional information including the diagnosis, treatment, and zoonotic potential of chlamydophilosis.
Neurologic disease in pigeons is often caused by toxic exposure or infectious disease (Table 5). Central nervous system signs can include torticollis and circling, ataxia, paresis, and even paralysis. Birds may be unable to prehend food, often pecking at and missing food items. The owner may also report the bird missing the perch when landing or even falling off of the perch.
|Table 5. Important causes of neurologic disease in the pigeon (De Herdt and Pasmans 2009, Hooimeijer 2006)|
|Viral disease||Herpesvirus||Weakness, ataxia, tremors|
|Paramyxovirus-1||Ataxia, tremor, paresis, complete or partial paralysis, incoordination of head movements, torticollis, and circling|
|Bacterial disease||Salmonellosis (paratyphoid)||Infection can localize in the brain and even the ear.
Source of infection is feral pigeons
|Streptococcosis||S. gallolyticus septicemia can lead to meningitis and/or encephalitis. Clinical signs can include complete paralysis or leaning on the forehead in an attempt to stand. Septicemia most common between January to August.*|
|Metabolic disease||Hypocalcemia||Ataxia, muscle fasciculations, seizure activity|
|Egg binding||Mechanical compression of nerves to the legs|
|Toxic exposure||Organophosphates||The most common intoxication observed in pigeons. Clinical signs can include mydriasis, salivation, tremors, tetany, paresis, diarrhea, and death|
|Heavy metals||Tremors, circling, seizure activity, and/or blindness|
|Dimetridazole, metronidazole||Overdose of these nitroimidazoles can cause ataxia, blurred vision, blindness, and weight loss|
|*Based on observations in Belgium (De Herdt and Pasmans 2009)|
Important rule-outs for conjunctivitis in the pigeon include Chlamydophila psittaci (see ornithosis complex) and Mycoplasma columbinum, only rarely reported in pigeons (Duizer et al 2010, Hooimeijer 2006). Pigeon fanciers sometimes call conjunctivitis “one-eyed cold”. A swollen, inflamed nictitans is also known as “the film” (Hooimeijer 2006).
|Table 6. Important causes of musculoskeletal disease in the pigeon (Harlin 2013, De Herdt and Pasmans 2009, Hooimeijer 2006)|
|Bacterial disease||Salmonellosis (paratyphoid)||Septic arthritis, especially in the elbow|
|Streptococcosis||Tenosynovitis, myositis, pectoral muscle necrosis, complete paralysis|
|Metabolic disease||Hypocalcemia||Pathologic fractures|
|Muscle damage||Secondary to overexertion|
|Leg band trauma|
|Paratyphoid, caused by Salmonella typhimurium var. Copenhagen is the most important bacterial disease of pigeons and doves. Transmission of the microbe is fecal-oral, with feral pigeons serving as a source of infection. Most infected birds remain asymptomatic carriers if the clinical signs of disease can be resolved. Clinical signs depend on the organ(s) affected and the extent of the lesions, but can include slimy green or bloody diarrhea, poor body condition, infertility or embryonic death, panophthalmitis with secondary blindness, abscess formation in the skin, exudative dermatitis, opisthotonus, arthritis, and sudden death. Extensive swelling of the elbow is an almost pathognomonic clinical sign and is sometimes referred to as “boils” by pigeon fanciers. The shoulder, triosseous canal, and joints of the leg can also be affected. Euthanasia of clinically affected birds is generally recommended, because treatment is very difficult and prolonged, and because survivors can become asymptomatic carriers. Extensive quarantine, sanitation, and measures to minimize stress should be performed for all remaining pigeons in the flock (De Herdt and Pasmans 2009, Coles 2007).|
|Table 7. Important causes of dermatologic disease in the pigeon (Harlin 2013, De Herdt and Pasmans 2009, Harlin and Wade 2009, Hooimeijer 2006, Tudor 1991)|
|Viral disease||Paramyxovirus-1||Malformation of feathers if PMV-1 occurs during molt|
|Poxvirus||Hypertrophic proliferation of the epithelium, predominantly around the beak and on the eyelids.|
|Parasitic disease||Lice||Pigeon lice are fairly common. Species can parasitize the feathers of the wings (Columbicola columbae) and tail (Campanulotes bidentatus) where they feed on feather dust, or feed on blood (Pseudolynchia canariensis). Although the damage to the feathers is minimal, the resultant restlessness in infested birds can be significant.|
|Mites||Megninia columbae, Falculifer rostratus, and Neoknemidocoptes laevis can create pinholes within the plumage. Knemidocoptes mutans can infest the skin, especially overlying the legs, causing broken feathers, scaly skin and legs, and baldness predominantly in the neck region.
Dermanyssus gallinae and Ornithonyssus sylviarum are blood-sucking mites.
|Ticks||Argas reflexus is a blood-sucking tick.|
|Toxic exposure||Benzimidazoles||Benzimidazole anthelmintics can cause feather abnormalities if given during molting|
|Trauma||Mutilation||Trauma is a common problem in crowded lofts. Columbids can be fairly aggressive, pugnacious birds, particularly during the breeding season|
|Exertion||Worn flight feathers are sometimes observed in racing pigeons|
|Pigeon poxvirus affects all age groups but clinical outbreaks predominantly occur in young pigeons. It is more common during seasons that promote the mosquito vector, however infection can also be spread from bird to bird as long as there is a defect in the skin for the virus to penetrate. Cutaneous and diphtheritic forms of poxvirus can appear separately or together as a mixed infection (Harlin 2013, De Herdt and Pasmans 2009, Wernery 2008, Rupiper 1998, Hooimeijer and Dorrestein1997):
A strong index of suspicion for poxvirus infection can be based on these characteristic lesions. Use cytology to confirm the presence of eosinophilic, intracytoplasmic inclusions known as Bollinger bodies for confirmation.
There is no treatment for poxvirus. Provide supportive care and administer antibiotics for secondary bacterial infection as needed. Protect flocks with a modified live, homologous vaccine (AviPro Pigeon Pox, Lohman Animal Health International; Colombovac PMV Paramyxo & Pox, Pfizer), beginning in birds as young as 4 weeks of age (Harlin and Wade 2009). Vaccines are administered directly into an epilated feather follicle on the lateral thigh or by subcutaneous injection. An inflammatory reaction produces a swelling with a yellowish-brown discoloration in the area 5-7 days later, and this indicates successful vaccination (Harlin and Wade 2009, Greenacre 2005). Vaccination can be a useful measure during a poxvirus outbreak, however care must be taken not to spread the infectious virus via the equipment used.
Note: Subcutaneous injections in racing pigeons are often made over the dorsal base of the neck (De Herdt and Pasmans 2009).
All dead pigeons should be necropsied with histopathology of tissues. Potential causes of sudden or peracute death in pigeons include (Bonfante et al 2012, De Herdt and Pasmans 2009, Stoute et al 2009, Coles 2007, Rupiper 1998, Hooimeijer and Dorrestein 1997):
- Adenovirus type II
- Herpesvirus (nestlings)
- E. coli septicemia (nestlings)
- Streptococcus gallolyticus septicemia
- Acuaria sp. (heavy infestations can cause severe anemia, high mortality rates)
In rare instances and especially in young birds, acute death can occur when the parasite invades large vessels. Virulent strains can also result in mortality rates as high as 50% although the course of disease is subacute to chronic.
- Metabolic disease like heat stress
- Toxic exposure
|Streptococcus gallolyticus can be a part of the normal gastrointestinal flora and is therefore considered a facultative pathogen. As long as S. gallolyticus bacteria are limited to the intestinal tract, no clinical signs are observed.
Septicemia caused by Streptococcus gallolyticus (previously known as S. bovis) can be observed in pigeons of all ages. Incidence of septicemia is highest between January and August in Belgium and may be highest in hens during the breeding season (De Herdt and Pasmans 2009). Acute or peracute death is the most common clinical finding. The most typical lesion consists of a large, well-circumscribed necrotic focus within the pectoral muscle, which can be visible through the skin. Other clinical signs commonly observed are related to tenosynovitis of the tendon of the deep pectoral muscle and/or septic arthritis of the shoulder, stifle, and hock joints. Affected birds may exhibit wing droop, inability to fly, and lameness as well as emaciation, polyuria, and green, slimy diarrhea. Complete paralysis or birds leaning on their head in an attempt to stand up may also be seen. Occasionally, wasting may be the only clinical expression of disease (De Herdt and Pasmans 2009, Hooimeijer and Dorrestein 1997).
Diagnosis can be suspected on the basis of clinical signs, however, definitive diagnosis relies upon isolation of S. gallolyticus; thus, necropsy is required. At necropsy, S. gallolyticus may be cultured from the liver, spleen, kidneys, and myocardium (De Herdt and Pasmans 2009).
Streptococcal septicemia can be difficult to treat, and antimicrobial therapy should be based upon sensitivity testing. Acquired resistance to macrolides, lincomycin, enrofloxacin, tetracyclines, and sulfonamides has been documented. Penicillin G, ampicillin, or amoxicillin can be used to treat empirically. Prevention is far superior to treatment, and relies upon quarantine, strict hygiene, and stress reduction (De Herdt 2009).
Important disease conditions in the pigeon often include parasitic diseases like lice and mites, roundworms, Hexamita columbae, and Trichomonas gallinae as well as bacterial diseases such as chlamydophilosis, staphylococcosis, salmonellosis or paratyphoid, and colibacillosis. Viral diseases, such as paramyxovirus-1, circovirus, and herpesvirus, are reported commonly in wild pigeons and sporadically in captive flocks.
By definition, pigeons maintained for show or racing purposes are kept as open flocks. Birds have frequent contact with pigeons from other lofts and infectious disease is common, particularly during the racing season. Predisposing factors for disease include overcrowding, inadequate husbandry practices, indiscriminate antibiotic use, failure to vaccinate, and racing birds that are not in proper condition (Hooimeijer 2006, Rupiper 1998, Hooimeijer and Dorrestein 1997). Once disease is symptomatic, the infection has generally peaked within a flock and management must generally focus on limiting morbidity and mortality. When the health of a flock is the goal, management often involves culling and necropsy of affected birds (De Herdt and Pasmans 2009).
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