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Author: Florina S. Tseng, D.V.M.
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OCW Zoological Medicine 2008
Pigeon and Passerine Medicine (2008)
F. Tseng, DVM
Cummings School of Veterinary Medicine at Tufts University

1. Learning Objectives

This section pulls together the main diseases and health issues of pigeons and passerines, both in captivity and in the wild. Color coded topics indicate learning objectives that the student should become familiar with. Cases will be presented in class to illustrate these topics.

2. Pigeons

A rock dove or common pigeon.
A rock dove or common pigeon.

Columbiformes include 42 genera, and over 300 species spread around the world. Our native species include the common rock dove and mourning dove.

  • Domestic vs. wild pigeons

  • Rock dove Columba livia is native to Europe, North Africa, and southwestern Asia. Non-native to North America.

  • Ornamental and sporting pigeons

2.1. Anatomy

  • Crop produces "crop milk" to feed young squabs

  • Ventriculus usually contains stones and other grit

  • Extensive venous plexus in neck makes jugular venipuncture difficult

2.2. Housing and Management

  • Pigeon lofts

  • Pelleted feeds, supplements

  • Quarantine

  • Sanitation

2.3. Clinical presentations

2.3.1. Neurologic problems

  • Avian paramyxovirus - Pigeon paramyxovirus , Newcastle disease (PMV-1), PMV-7

    • Probably infected orally or through aerosal transmission

    • Virus spreads to kidneys and/or the CNS

    • Clinical signs include PU/PD, CNS signs including torticollis, complete or partial paralysis

    • Morbidity high, mortality low

  • Trauma

  • Eastern, Western and Venezuelan equine encephalomyelitis

  • St. Louis encephalitis

  • West Nile Virus

  • Toxicity

  • Hypocalcemia in breeding females

2.3.2. Skin problems

  • Ectoparasites

  • Pigeonpox


  • 'Typical' pox infection associated with vector availability

  • Atypical pox infection results in wart-like lesions that are predominantly located on the body or wings; these lesions bleed heavily when damaged

2.3.3. Wing and leg abnormalities

  • Splay leg

  • Nonseptic arthritis

  • Bumblefoot

  • Trauma

2.3.4. Upper respiratory and ocular abnormalities

  • Chlamydophila psittaci (distinct pigeon serovar)

    • Usually results in respiratory disease

  • Trichomonas

    • Caused by T. gallinae

    • Pigeon is primary host

    • Extremely common in domestic pigeons

    • Severe lesions and clinical problems usually seen in young pigeons

    • Shed through saliva and crop milk

    • Cause lesions in the oropharynx that can lead to starvation due to inability to ingest food

    • Diagnosed from crop swabs and identifying organisms microscopically

    • Can be treated with carnidazole, metronidazole

2.3.5. Upper GI signs

  • Sour crop

  • Candida albicans


  • Capillaria

    • Note that toxicity has been observed with fenbendazole and albendazole in pigeons and doves. These anthelmintics should be avoided in Columbiformes, or should only be used with caution.

2.3.6. Other GI abnormalities

  • PMV-1

  • Adenovirus

    • Type 1 results in severe intestinal damage and can spread systemically

    • Type II clinical signs minimal, leads to acute death

  • Herpesvirus - inclusion body hepatitis, pigeon herpes encephalomyelitis

  • Rotavirus in young pigeons

  • Circovirus

  • Salmonella typhimurium

    • Pigeon-specific serotype spread through oral transmission

    • Can result in asymptomatic carriers

    • Clinical signs are usually associated with enteritis but may evolve to formation of abscesses and granulomas , arthritis of the legs and wings

  • Chlamydophila

  • Hexamita columbae

  • Cocciodiosis

    • Eimeria sp.

    • High incidence, low pathogenicity

    • Can develop immunity to infection

    • Clinical problems mostly seen in young birds

    • Heavy infestations treated with sulfa drugs

2.4. Preventative Medicine

Vaccines are available for pigeon poxvirus, avian paramyxovirus type 1-pigeon, and salmonella . Routine vaccination is often done in late summer. Newly hatched birds are vaccinated for pox at the end of their first July. Flocks should be screened for salmonella and parasites just before the breeding season. Pigeons are often routinely treated for trichomoniasis just before the first clutch hatches.

3. Passerines

Passeriformes - Passerines

Jays, Crows
Titmice, Chicadees
Thrushes, Robins
Pipits, Wagtails

Blackbirds, Orioles

Wild passerines represent a very large and diverse group, in which captive and wild finches are only a small part. Many of the disease syndromes are similar, and some diseases can be shared between wild and captive birds in the same family.

Finches are often kept in large groups as ornamental or breeding birds (or both). Canaries are really just large finches and diseases can be shared between the two. In canaries, kept for their lovely singing voices, the male is the best singer . Vocalization is intensified in the spring during the breeding season. A sign of illness in a male canary is often the cessation of his usual singing.


3.1. Restraint and handling

"I didn't examine the bird because I thought it might die in my hands." This gets you nowhere. Proper and gentle restraint is essential to physical examination and assessment, even of the smallest patient. Hold the bird in one hand, control the head, and do not restrict chest movements enough to prevent sternal excursions. Perform exam quickly but thoroughly, maintaining awareness of stress, dyspnea, and/or change in mental status.


3.2. Anatomy and physiology

  • High basal metabolic rates influence nutritional needs, fluid administration, and drug dosaging

  • Most passerines have three forward toes and one rear toe (anisodactyl) though some have zygodactyl toes (two front, two rear), e.g. woodpeckers to enable them to cling vertically onto trees

  • Anatomy of digestive tract varies by species' feeding habits, e.g. seedeaters have powerful bills and a muscular ventriculus to grind seed

  • Singing ability highly developed and related to anatomy of the syrinx

  • Highly efficient respiratory system

3.3. Housing

  • Can be kept as individual pet birds or in ornamental or breeding aviaries

  • Mixed ornamental aviaries usually provide shelter and outdoor flight caging

  • Breeding aviaries are generally indoors, with housing dependent on the species

3.4. Diet and husbandry

  • Passerines can be granivorous (seed-eating), nectivorous, frugivorous, insectivorous, omnivorous, or even carnivorous

  • Most commercial diets are seed based so be aware of associated nutritional deficiencies, e.g. hypovitaminosis A, hypocalcemia etc.

  • Passerines presented for rehabilitation to the wild must be given appropriate diets to encourage self-feeding

    • Seed eaters (sparrows, finches, others): wild bird seed, suet, thistle for small birds

    • Omnivores (robins, crows, jays, others): wild bird seed, suet, berries, canned or soaked dry cat food, mealworms

    • Nectivores (hummingbirds): commercial hummingbird diets are available

    • Insectivores (swallows, swifts, others): have difficulty self-feeding in captivity because they usually eat insects on the wing. May handfeed mealworms rolled in Nutrical® and dusted with calcium powder.

3.5. Diagnostic Procedures

  • Fecal examination

  • Crop swabs

  • Blood samples (generally use right jugular vein)

  • Necropsy

3.6. Non-infectious diseases

  • Feather cysts are common in canaries


  • Trauma

    • Toe constrictions

    • Broken limbs

    • Predator and impact trauma (wild birds)

  • Amyloidosis (Gouldian finches)

  • Hepatic lipidosis can be seen in some finches and may be associated with inadequate exercise and high-energy food intake

  • Metabolic bone disease occasionally seen in free-living crows. May involve inappropriate food choices by parent birds (garbage scavenging), or environmental contaminants interfering with normal calcium metabolism.

  • Egg-binding

  • Vitamin deficiencies

    • Hypovitaminosis A from seed diet; is also seen as a genetic defect in recessive white canaries

    • Some insectivores or frugivores cannot synthesize Vitamin C and depend on dietary sources for this vitamin.

    • Vitamin D3 and/or hypocalcemia may be seen during the breeding and egg laying season

  • Toxicosis

    • Avocado can be toxic to some passerine birds

    • Green almonds have been toxic to some birds (cyanide)

    • Ethanol toxicity in free-ranging passerines, especially cedar waxwings, following ingestion of certain fermented fruits


3.7. Infectious diseases

3.7.1. Viral

  • Poxvirus

    • Cutaneous, diphtheric, and septicemic forms can be seen in canaries

    • Preventative vaccines available, given in wing web

  • Polyomavirus

    • Seen in finch aviaries

    • Causes young nestling mortality

  • Paramyxovirus 1, 2, and 3

    • Seen in finches and results in CNS signs

  • Herpesvirus/cytomegalovirus

    • Conjunctivites, respiratory problems

  • Adenovirus West Nile virus

An outbreak of West Nile virus (WNV) in metropolitan New York and surrounding areas during the Fall of 1999 brought a new disease to birds and mammals in the Western Hemisphere. WNV is a flavivirus closely related to St. Louis encephalitis virus, Kunjin virus and Murray Valley encephalitis. It is spread by mosquitoes (Culex and Aedes sp.) and ticks similar to Eastern Encephalitis virus.

WNV was first isolated in Uganda in 1937. It is considered endemic in Africa, the Middle East and western Asia with periodic outbreaks in Europe. Studies in Egypt in the 50's demonstrated a strong susceptibility of crows to this virus. This past year an outbreak occurred in Israel in domestic geese with significant mortality. The virus isolated in NY is identical to the strain found in the 1998 Israeli outbreak.

In August of 1999, people in NY City were diagnosed with an arboviral encephalitis similar to St. Louis encephalitis. At the same time birds (especially crows ) began dying in the NY metropolitan area: specifically noted were some valuable exotic birds dying of encephalitis at the Bronx Zoo. The pathologist at the zoo (McNamara) made the link and a diagnosis of the West Nile Virus eventually was confirmed. No one knows how it got into this country. On the basis of DNA analysis it is suspected to have originated in the Middle East.

There were 7 human deaths in the 1999 outbreak, 62+ illnesses, and more than 1900 exposures (in Queens alone). Thirteen horses' deaths and over 22 illnesses were attributed to WNV on Long Island. Countless bird deaths also occurred in this outbreak involving 18 different native species. Crows are clearly the most susceptible. The disease continues to progress across and United States, Canada, and into Latin America, affecting crows and other birds, horses and people. More information can be obtained in the Supplemental Readings or directly from the National Wildlife Health Center .

Clinical signs

Clinical signs in birds are consistent with encephalitis and might include weakness, stumbling, trembling, head tremors, inability to fly/walk, and lack of awareness. Histopathologic lesions are characteristic of a non-suppurative encephalitis characterized by perivascular cuffing of mononuclear cells, predominantly lymphocytes, and multifocal neuronal satellitosis and neuronophagia. Severe myocarditis has also been observed. Rule outs should include Eastern Encephalitis.

Clinical signs in horses include anorexia, depression, listlessness, fever, hind limb weakness, flaccid paralysis of the lower lip, impaired vision, ataxia, head pressing, aimless wandering, convulsions, dysphagia, circling, hyperexcitability, paresis, coma or death. (R/O rabies).

3.7.2. Bacterial

  • Chlamydia - considered resistant. Look for if exposed to psittacines

  • Mycoplasma - EMERGING DISEASE in wild finches

    • First seen in the mid 90's in the mid-Atlantic states

    • Has since spread throughout the eastern US

    • Clinical signs range from mildly swollen eyelids to severe conjunctivitis with mucoid discharge

    • Affected birds may have visual impairment leading to starvation and vulnerability to predator attacks

    • Treated with tetracycline ophthalmic drops or ointment for 5 days and oral tylosin as drinking water source for at least 21 days

  • Staphylococcus, Streptococcus

  • Enterobacter, E. coli, Salmonella, Citrobacter, Yersinia, Klebsiella, Pasteurella, Haemophilus, Campylobacter, Pseudomonas

  • Listeria (esp. canaries)

  • Mycobacterium

3.7.3. Fungal

  • Candida

  • Aspergillus

  • Cryptococcus spp. often recovered from feces, pathogenic?

  • Avian gastric yeast


3.7.4. Parasitic

  • Protozoa including cochlosoma, Trichomonas, Giardia, and Coccidia (esp. Atoxoplasma )

    • Atoxoplasma is a disease of young canaries resulting in debilitation, diarrhea, neurological signs and death. Mortality can be as high as 80%

  • Cestodes

  • Nematodes including Ascarids, Capillaria, Spirurids, and Syngamus

    • Syngamus trachea (gapeworm) found in outdoor aviaries or in wild passerines. Earthworms may act as transport hosts. May be seen with tracheal transillumination

  • Trematodes

  • Acanthocephalans

  • Air Sac Mites ( Sternostoma tracheacolum )

    • Most commonly seen in Australian finches

    • Clinical signs include dyspnea, coughing, sneezing, loss of voice

    • Mortality low

  • External parasites including mites and lice

  • Hemoparasites including: Haemoproteus, Leucocytozoon, Trypanosoma, Plasmodium, Atoxoplasma, and microfilaria

4. Toucans (Ramphastids)

  • Woodpecker family

  • Tropical birds

  • Bill composed of outer keratin covering with inner network of air-filled trabeculae

  • Common problems

    • Beak fractures

    • Diabetes mellitus

    • Yersinia pseudotuberculosis

  • Hemochromatosis

Hemochromatosis is the iron storage disease of mynah birds, birds of paradise, starlings, quetzals, ramphastids (toucans) and occasionally other birds. The etiology in most species is uncertain and still under investigation. Proposed causes include a genetic defect in iron absorption or metabolism, or a dietary cause. In some species there appears to be an extremely efficient intestinal iron absorption mechanism: birds of paradise absorb 90% of dietary iron, humans only 10%. Further examination of the natural environment of these birds may reveal a dietary driven evolutionary adaptation to allow increased intestinal absorption of iron.

The disease results in an abnormal accumulation of iron pigments in hepatocytes (and other tissues such as myocardium, lung, kidneys, etc.), hepatic fibrosis, hepatomegaly, ascites resulting in severe abdominal distention, dyspnea, anorexia, and finally death.

  • Clinical signs - Birds usually present cachectic, in severe respiratory distress with pronounced ascites. Ramphastids (toucans) often have very vague signs and may not develop ascites.

  • Diagnosis is made based on signalment, clinical signs, radiographs and liver biopsy (total serum iron concentration is not considered diagnostic).

  • Treatment includes abdominocentesis to relieve pressure (one time emergency only), diuretics, steroids, and phlebotomy (1% body weight in ml, once weekly) and dietary management. The use of deferoxamine, an iron chelating agent used in people, may be helpful and can be used on a chronic basis. The prognosis is always guarded.

  • Prevention of this disease in susceptible species has been most successfully accomplished through feeding low iron diets. This is critically important for maintenance of these birds in captivity.

5. References and Resources

5.1. Pigeon references

Altman, Robert B., et al. Avian Medicine and Surgery . Philadelphia. W.B. Saunders Co., 1997. Chapter 50

Beynon, Peter H. Manual of Raptors, Pigeons and Waterfowl. BSAVA, 1996.

Cross, Garry. Paramyxovirus-1 infection (Newcastle disease) of pigeons. Seminars in Avian and Exotic Pet Medicine , Vol. 4, no. 2, 1995: pp. 92-95.

Dorrestein, Gerry M. Viral infections in racing pigeons. 1992 Proceedings of the Association of Avian Veterinarians , pp. 244-257.

Dorrestein, Gerry M. Passerine and softbill medicine. AAV Clinical Forum, March - May 2005: pp 3-13.

Harrison, Gregg J. and Teresa L. Lightfoot. Clinical Avian Medicine . Palm Beach, FL: Spix Pub., c2006. Chapter 37.

Marshall, Robert. Management of pigeon diseases. 1990 Proceedings of the Association of Avian Veterinarians , pp.122-135.

Ritchie, Branson W., et al. Avian Medicine: Principles and Application . Lake Worth, Fla., c1994: Chapter 44.

Rupiper, D.J. Diseases that affect race performance of homing pigeons, Parts 1 & 2. Journal of Avian Medicine and Surgery , 12 (2,3), 1998.

Tudor, DC. Pigeon Health and Disease . Ames: Iowa State University Press, 1991.

Tully, Thomas N., Martin P.C Lawton, and Gerry M. Dorrestein. Avian Medicine . Boston Butterworth. 2000. Chapter 14.

5.2. Passerine references

Altman, Robert B., et al. Avian Medicine and Surgery . Philadelphia. W.B. Saunders Co., 1997. Chapter 49.

Bauck, Louise. Survey of diseases of the Lady Gouldian finch. Proceedings of the Annual Conference of the Association of Avian Veterinarians , New Orleans, LA, 1999: 204-212.

Dorrestein, Gerry M. Virus infections in passerines with special reference to a coronavirus-like infection in canaries ( Serinus canaria ). Proceedings of the Annual conference & Expo of the Association of Avian Veterinarians , August 28-30, 1996: pp. 171-176.

Fischer, John R. et al. Mycoplasmal conjunctivitis in wild songbirds: the spread of a new contagious disease in a mobile host population. Emerging Infectious Diseases , 3 (1), 1997.

Harrison, Gregg J. and Teresa L. Lightfoot. Clinical Avian Medicine . Palm Beach, FL: Spix Pub., c2006. Chapter 39.

Kollias GV, et al. Experimental infection of house finches with Mycoplasma gallisepticum. Journal of Wildlife Diseases , 40(1), 2004: pp. 79-86.

Ritchie, Branson W., et al. Avian Medicine: Principles and Application . Lake Worth, Fla., c1994: Chapter 43.

Tully, Thomas N., Martin P.C Lawton, and Gerry M. Dorrestein. Avian Medicine . Boston Butterworth. 2000. Chapter 7.

Weingartl HM et al. Experimental West Nile Virus Infection in Blue Jays ( Cyanocitta cristata ) and Crows ( Corvus brachyrhynchos ). Veterinary Pathology , 41 (4), 2004: 362-370.