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1. Learning Objectives
- Be familiar with the important viral diseases in pet birds, poultry and wild birds presented in this section
- Gain an appreciation for the interaction of wild and domestic/captive birds and implications for disease transmission
- Know in detail the following diseases, including clinical
presentation, diagnosis and treatment/management options:
- Paramyxoviruses
- Avian Influenza
- Herpesvirus (Pacheco's)
- Polyomavirus
- Duck viral enteritis
- Proventricular dilatation syndrome
- Psittacine beak and feather disease.
- Know the basic clinical presentation, diagnostic workup and treatment for non-specific hepatitis in a pet bird
2. Introduction
Due to the economic importance of the poultry industry, the study of viral diseases in this group of birds has been intense and is extremely sophisticated. This body of knowledge is very useful in broadening our understanding of viral diseases in other birds, especially pet birds. Many of the pathogenic poultry viruses are similar to those that cause disease in pet birds, and methods of diagnosis and control used in poultry can often be adapted for use in pet birds (e.g. vaccinology).
The following viruses are grouped according to the primary system involved in the disease process. It is important to recognize that these viruses are systemic diseases and are capable of producing clinical disease in many different body systems.
3. Avian Paramyxoviruses
Other names for this disease:
- Newcastle Disease (ND)
- Avian pneumoencephalitis
- Asiatic Newcastle disease
- Velogenic viscerotropic ND (VVND)
- Pigeon paramyxovirus
There are 9 different strains (serotypes) of avian paramyxovirus, the most important of which is PMV-1 or Newcastle disease. This virus often presents as a respiratory disease in poultry, however it should be thought of as a systemic disease, often involving the CNS, the gastrointestinal tract and/or the respiratory tract. Clinical manifestations of Newcastle disease in birds is remarkably similar to that of canine distemper virus in dogs, both viruses are taxonomically related.
3.1. Newcastle Disease (ND) or PMV-1
 High morbidity and mortality in an outbreak of
Velogenic Viscerotropic Newcastle Disease.
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ND virus (NDV) is a ubiquitous virus that can be isolated from many species of wild and domesticated birds. In addition to chickens - turkeys, peafowl, guinea fowl, pheasants, quail and pigeons are naturally susceptible. A wide range of virulence is encountered in different strains of virus. Identification is based on the antigenic make up of neuraminidase and hemagglutinin receptors on the envelope. NDV cause a wide spectrum of disease in domestic fowl and pet and wild birds.
Lentogenic, mesogenic and velogenic strains of NDV are described in the literature. These terms indicate differences in viral pathogenicity using the chicken as the index species. Lentogenic NDV causes clinically non-apparent disease in chickens but this same virus may kill canaries. Conversely, velogenic NDV causes relatively mild disease in Amazon parrots but this same virus would produce lethal disease in a flock of egg laying hens with 100% mortality. Mesogenic NDV is the most common form of virus isolated from commercial poultry flocks. Many outbreaks present with mild or atypical lesions. This is the result of the common practice of vaccinating commercial poultry with modified live NDV vaccine. The vaccine virus sometimes reverts to mildly virulent virus that may produce clinical disease. Commercial NDV vaccines are usually administered in the drinking water or by aerosol.
Velogenic NDV (VVND) is the most virulent form of the virus. It was introduced onto the U.S. through importation of wild psittacine species subsequently sold as pets. The susceptibility to this virus among psittacines varies with cockatoos being the most susceptible. Parakeets are comparatively refractory to infection. Psittacines infected with VVND show variable clinical signs which include lethargy, diarrhea, muscle tremors, and opisthotonos. Any psittacine showing CNS signs with concomitant diarrhea and respiratory signs should be considered a potential case of velogenic Newcastle disease; cases of VVND are REPORTABLE to the USDA.
Pigeon paramyxovirus (PMV-1 pigeon, PPV) was first seen in Europe and Great Britain in the early 1980s. It has been observed in pigeons in the U.S. since 1984. Paramyxovirus is very common in pigeons, both wild and domestic. Show and racing pigeons are the most common species infected with pigeon paramyxovirus. This form of the virus is also infectious to chickens, Common Blackbirds and House Sparrows. Serologic testing can be performed to confirm the pigeon paramyxovirus. Several vaccines are available to assist in controlling the pigeon disease in captive flocks.
PMV-1 in pet birds is most often diagnosed as VVND entering the country via smuggled amazon parrots, and threatening the nations poultry industry. An outbreak in psittacines was traceable to a disreputable Houston dealer and involved birds in Indiana, Illinois, Michigan, and Texas (1991). A recent outbreak was identified in a Missouri pet bird facility killing Double Yellow- Headed Amazon parrots (1996). Poultry were not affected by either of these cases. VVND should be suspected in cases of recently acquired or exposed birds with peracute death or clinical signs of neurologic disease in combination with GI and/or respiratory disease. Such cases should be reported to the USDA for further investigation.
3.1.1. Clinical signs
3.1.1.1. Mesogenic virus in chickens
- Catarrhal nasal exudate
- Chicks less than a few weeks old show respiratory distress followed by diarrhea and neurological signs ("star gazers").
3.1.2. Diagnosis
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A suspicion of ND can often be made on the basis of history, clinical signs and gross and microscopic lesions which include: cloudy air sacs with frothy, yellow air sac contents, chronic infection may result in dry caseous exudate in the air sacs. Non-suppurative encephalitis is one of the most consistent microscopic lesions.
VVND usually shows hemorrhagic, ulcerative and necrotizing lesions in gastrointestinal epithelial and lymphoid tissues. It is impossible to confirm a diagnosis of ND without serologic or virologic confirmation. These include: HA and HAI tests, virus neutralization, FA tests using conjugated anti-NDV serum and demonstration of rising anti-NDV activity in pooled sera.
3.1.3. Prevention
Many ND vaccines are available. The commercial vaccines are usually modified live type that are administered by aerosol to large numbers of birds. Other vaccines are administered by eye drop or drops in the nares. Killed, oil-emulsified vaccines are also available for parenteral administration.
3.2. Other Avian Paramyxoviruses
PMV-3 is the most common strain found in pet birds and usually produces a mild self-limiting disease that is rarely diagnosed. The PMV-3 strain can cause severe disease in Neophema (Bourke's Parakeet), producing marked neurologic, GI and respiratory signs. Paramyxoviruses also occur frequently in wild birds and usually produce a neurologic disease, but often involving other systems as well. An outbreak in 1992 among Double-Crested Cormorants in the Midwest involved up to 90% mortality. The strain isolated in this outbreak was classified as a neurotropic form of VVND and was also seen in a turkey flock in the area.
 Newcastle Disease in a Double-crested
Cormorant.
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4. Avian Influenza
(AI, Fowl Plague) Avian influenza is caused by an orthomyxovirus of variable pathogenicity. Two principle strains of virus have been identified. Conventional avian influenza (AI) is usually seen in domestic turkeys and ducks and causes respiratory disease that rarely exceeds a 15% mortality. Chickens are less often affected and show mild clinical signs. Highly pathogenic forms of AI (fowl plague) is a much more virulent disease that causes high morbidity and mortality in chickens. Avian influenza virus differs from mammalian influenza virus in having the ability to infect and replicate in epithelial cells lining the gastrointestinal tract.
At least 17 different strains of avian influenza virus have been isolated from a variety of birds which include chickens, turkeys, Ring-Necked Pheasants, and Starlings. Migratory waterfowl should always be considered as a potential source of virus when and outbreak of AI occurs in poultry.
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4.1. Highly pathogenic avian influenza (fowl plague)
This disease is caused by more virulent strains of AI virus. In October of 1983 several point mutations of avian influenza virus occurred (antigenic drift) resulting in a severe epidemic in domestic poultry in the eastern U.S. The economic significance of this seemingly trivial biologic event was emphasized by a cost of more than sixty million dollars paid in indemnities for millions of chickens slaughtered in an effort to control the disease. In February of 1993 H5N2 avian influenza virus was identified in a commercial egg laying flocks in New York, New Jersey and Pennsylvania. This disease is REPORTABLE to the USDA APHIS.Some strains are ZOONOTIC (H5N1).
4.2. Clinical Signs
4.2.1. Low to moderately virulent virus in chickens
- Coughing, "sneezing", respiratory rales and lacrimation, anorexia, lethargy and emaciation.
- Egg laying hens may show a drop in egg production.
- Sinusitis with infraorbital swelling have been reported in some outbreaks however, this finding my be due to secondary infection with Hemophilus paraganinarum (coryza).
- Sinusitis is a common finding in ducks with avian influenza.
- Diarrhea, edema of the head and nervous signs are occasionally observed.
 Chicken with Highly Pathogenic Avian
Influenza
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4.2.2. Highly pathogenic influenza virus in chickens
- Facial edema with focal cyanosis and hemorrhage of the comb, wattles and non-feathered skin (probably the result of virus induced DIC)
- Focal mucosal hemorrhage of the proventriculus occurs similar to lesions seen in VVND but in fowl plague this lesion is not associated with submucosal lymphoid tissue necrosis.
4.3. Diagnosis
Confirmation of AI must be made on the basis of virus isolation and identification. Serologic information can be useful but seropositive birds may be the result of a previous, sub-clinical infection with a low virulence AI virus.
4.3.1. Gross lesions
These vary widely depending on the strain of the virus involved in the outbreak. Reddened tracheal mucosa, sinusitis, cloudy air sacs and conjunctivitis may be the only lesions seen in outbreaks of low virulence AI.
Highly pathogenic strains of AI will produce diffuse petechia and fibrinous exudate on abdominal serosal surfaces. Mucosal hemorrhages in addition to GI tract can also be seen. Microscopic lesions may be helpful in establishing a diagnosis. These consist of perivascular lymphocytic cuffing in myocardium, lungs, brain, liver and wattles. Additionally, necrosis of splenic lymphoid follicles and pancreatic acinar cells has been seen in highly pathogenic AI.
5. Laryngotracheitis virus (LT)
Laryngotracheitis is an acute, highly contagious, respiratory disease of chickens caused by a herpes virus. The disease is principally seen in chickens and a few rare reports describe an LT-like disease in pheasants and peafowl. Amazon tracheitis virus is a related herpes virus that occasionally causes similar disease in psittacines.
5.1. Clinical Signs
- Nasal discharge, "coughing", gasping, dyspnea and expectoration of blood tinged mucus.
- Morbidity is high but mortality rarely exceeds 20%.
5.2. Diagnosis
A positive diagnosis can usually be made on the basis of gross and microscopic lesions.
 Gross appearance of LT
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Gross lesions are confined to the tracheal mucosa and include mucoid and hemorrhagic exudate in addition to fibrinous and heterophil inflammation. Intranuclear, eosinophilic inclusion bodies are usually seen in sloughed tracheal epithelial cells. These inclusions may be difficult to identify forty eight hours after first signs are observed since the damaged tracheal mucosa has been sloughed and is in a regenerating phase.
6. Infectious Bronchitis (IB)
This is an upper respiratory disease only seen in chickens that is caused by a corona virus. All ages are susceptible but disease is most severe in baby chicks. In addition to respiratory disease, this same corona virus can cause injury to the kidney and oviduct. Surface receptors on renal and oviduct cells may be similar due to the embryonic derivation of these tissues from a common primordial tissue.
6.1. Clinical Signs
- High morbidity and negligible mortality in chicks under 4 weeks of age. These birds will generally show respiratory signs of coughing, sneezing with nasal and ocular discharge.
- So called "nephrogenic" strains of virus will result in mortality exceeding 50% in young chicks.
- In older birds IB may be so mild as to go unnoticed.
- Laying hens may show a precipitous drop in egg production. Recovered hens often lay malformed eggs with roughened shells.
6.2. Diagnosis
A rising IB antibody titer with clinical signs and gross lesions consistent with IB are the usual criteria for a positive diagnosis. Gross lesions in adult chickens are usually non-specific and consist of mild air sacculitis. Rarely, caseous mucus may be found in the bronchi. Nephrogenic IB results in swollen kidneys with a serpentine, yellow brown pattern on natural surfaces due to the formation of intra-tubular uric acid crystals.
6.2.1. Differential Diagnosis
Mild forms of Newcastle disease or avian influenza can mimic infectious bronchitis. Also consider laryngotracheitis, mycoplasma and chlamydia.
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6.3. Prevention
Modified live vaccines are available. IB vaccines are often combined with Newcastle disease vaccines. These are usually administered as an aerosol or in the drinking water. Killed, oil-emulsified vaccines are also available for parenteral administration to individual birds.
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REMEMBER other viruses also involving the respiratory system: |
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7. Psittacine Hepatitis Complex
The clinical appearance of hepatitis in birds is fairly consistent regardless of the etiology. Clinical signs in pet birds include: Anorexia, vomiting/regurgitation, diarrhea, change in color of feces (bright green, yellow) and often urates as well (green or yellow biliary pigments). There is rarely jaundice. Birds may appear dyspneic from an enlarged liver or ascites producing a mass effect in the coelom. Neurologic signs may also be present with hepatoencephalopathy.
Approach to diagnosis should include history, physical exam (enlarged liver, ascites), CBC, blood chemistry (including bile acids, AST) and radiographs.
Differential diagnosis for psittacine hepatitis should include the viral diseases (herpesvirus, polyomavirus, adenovirus, reovirus) plus: bacterial hepatitis (mycobacteria,salmonella, other gram negative bacteria), parasitic hepatitis (coccidia, trematodes), chlamydiosis, toxic hepatitis (aflatoxins, lead), and hepatic lipidosis.
General treatment of viral hepatitis involves isolating affected birds and providing supportive care, including: fluid therapy, nutritional support, lactulose, and antibiotics for primary or secondary bacterial infections. Aviary management with identification of chronic subclinical carriers, etc. may be very difficult, but will be crucial. Vaccination for viral causes will become more important in the future.
Viral hepatitis in psittacine birds
Hepatitis in pet birds is a common clinical condition caused by several different viruses. There are 4 main viruses known to be responsible for this condition. Three of the four main psittacine hepatitis viruses and chicken adenovirus are characterized by the presence of inclusion bodies:
8. Herpesvirus
8.1. Psittacine Herpesvirus Hepatitis (Pacheco's disease)
Psittacine herpesvirus was first described by Pacheco and Bier in 1930-31 as a disease in Brazilian parrots = "Pachecos disease".
All psittacines are susceptible to this virus to a variable degree. There is often very high mortality in flock outbreaks. A report of an outbreak in a flock of 75 mixed psittacines resulted in 24 animals dead in 19 days! This is a devastating disease.
8.1.1. Clinical signs
Initially one may see sudden death without any clinical signs. However, signs that do consistently appear include anorexia, depression, and yellow mustard diarrheic feces.
8.1.2. Diagnosis
Diagnosis can be made based on clinical signs of hepatitis and epidemiological evidence of exposure (see below). Due to the peracute nature of this disease, necropsy of a dead bird often leads to diagnosis of a flock problem. Classic pathologic features include intranuclear eosinophilic inclusions and focal hepatic (and splenic) necrosis.
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8.1.3. Treatment
Although supportive care is the primary treatment available, sick birds rarely respond. Quarantine of sick birds is essential! A flock can be treated with Acyclovir for a minimum of 7 days. Birds that are already sick often do not respond. There was a vaccine (killed) available for this disease. However, due to some serious problems with the adjuvant in the vaccine it has been withdrawn.
8.1.4. Epidemiology
The epidemiology of this disease can make it difficult to manage. Classically, asymptomatic carriers have been shown to be the culprit in outbreaks. These carriers may incubate the disease for up to 2 years before shedding it. Historically Patagonian and Nanday conures have been implicated, although other birds may serve as carriers. Infection is spread initially by asymptomatic carriers but may be disseminated through human caretakers. It is felt that various forms of stress induce shedding of the virus in the feces. There is at present no sure way to identify carrier birds, or even birds that are responsible for an outbreak. In one study of 70 psittacines (mostly African Grey parrots and amazons), 30 were seropositive without any signs of disease! Amazons, cockatoos and macaws are very sensitive and often do not survive infection. Recovered birds may have lifelong immunity (low serum titer) but it is unclear whether these birds are carriers.
8.2. Other Avian Herpesviruses
Herpesviruses are double-stranded DNA viruses. In birds at least 8 serotypes have been identified involving 10 recognized diseases. As with other herpesviruses, latency is common. The following herpesviruses have been identified in birds:
- Hepatitis virus (Pacheco's), one main serotype
- Amazon tracheitis virus
- Budgie herpes virus?
- Cutaneous herpesvirus in cockatoos and macaws and amazons
- Laryngotracheitis virus and Marek's disease in chickens
- Duck plague in ducks, geese and swans (IMPORTANT)
- Pigeon herpes
- Falcon herpes
- Owl herpes
- Inclusion body hepatitis in cranes
- Stork herpes
- Cormorant herpes
9. Papovavirus
The family of papovaviruses includes cutaneous papillomaviruses and polyomaviruses commonly known to cause "budgerigar fledgling disease," a form of "French molt". Polyomaviruses cause feather dystrophy as well as classic hepatitis including intranuclear basophilic inclusions in the liver, spleen, kidney and many other tissues. Hydropericardium may also be seen along with an enlarged heart, enlarged pale congested liver with multiple pinpoint foci, and congested kidneys.
The disease chiefly effects young birds, budgies, lovebirds and other larger psittacines, but also may affect adults. This virus is also an important disease in finches. However, it is now felt that different strains of the virus are involved in finches, budgies, and larger psittacines and that these strains should not cross infect these groups. Polyomavirus in larger psittacines has become a very important and increasingly more common cause of fatal hepatitis in young birds across the country. These birds are nearly always captive bred birds which has made this recent phenomenon of great concern to American breeders.
9.1. Clinical signs
Clinical signs will vary with species and age of the bird. Poor/abnormal feather growth is seen most commonly in budgies. Other birds develop subcutaneous hemorrhages, depression, anorexia, weight loss, decreased crop motility, regurgitation, diarrhea, dehydration, dyspnea, ataxia/paresis/paralysis, polyuria, or peracute death.
9.2. Diagnosis
Diagnosis can be made based on antibody tests (virus neutralization), and a PCR test detecting antigen in feces and blood, and/or on post-mortem. It is recommended that both blood and cloacal swabs be submitted for testing in an aviary situation, preferably in serial sample submissions. The PCR test can also be performed on environmental samples (swabs of cages, rooms, bowls, etc.) to detect presence of the virus.
 Acute hepatic necrosis seen with polyomavirus
infection
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9.3. Treatment/Epidemiology
Treatment is symptomatic. Management of affected animals is critical in controlling or eliminating the disease in a flock situation. Vaccination is available to assist in managing this devastating disease and is recommended in aviary settings and for young birds leaving the aviary. Identification of the source of infection is very important. Recovered adults and parent birds may be implicated as subclinical carriers. Birds with persistently high titers (FA virus neutralization test) are probably carriers. Recent studies on budgies have shown that seropositive birds under the age of 2 years, including nestlings, are responsible for transmitting the disease. Removal of these birds from the breeding flock will eliminate the spread of infection to subsequent generations. Non-carriers achieve only short-lived titers. Virus may persist in the environment for a long period of time. The incubation period is felt to be 2 weeks or greater.
10. Adenovirus
Adenovirus is well described in poultry (hepatitis, aplastic anemia, egg drop syndrome), turkeys (hemorrhagic enteritis), quail (bronchitis) and pheasants (marble spleen disease). It has been described in a variety of psittacines. Classic pathologic lesions include intranuclear basophilic inclusions with diffuse hepatic necrosis. Pancreatitis, conjunctivitis, renal failure, diarrhea and encephalitis may also seen. Inclusion bodies may also be seen in renal epithelial cells.
10.1. Inclusion Body Hepatitis of chickens (IBH)
Over 20 different adenoviruses have been isolated from domestic fowl but few of these agents have been associated with spontaneous disease. In 1963, a disease was reported in chickens which produced acute mortality associated with severe hepatitis. IBH virus has also been linked with marrow aplasia and anemia. A previous immunosuppressive event, possibly related to avian leukosis, Marek's disease or infectious bursal disease may predispose birds to either of the above syndromes
10.1.2. Diagnosis
Gross lesions consist of a pale, swollen liver with subcapsular pin-point hemorrhagic foci. Bone marrow is pale and the peripheral blood is thin, pale and watery suggestive of anemia. Microscopic lesions consist of hepatocellular necrosis with occasional intranuclear inclusion bodies.
11. Reovirus
Reoviruses can effect many different organ systems including the liver. It is well studied and characterized in chickens (3-5 serotypes identified). It is also seen in pigeons and causes tenosynovitis in chickens and diarrhea in turkeys. This disease is not well understood in psittacines and is rarely diagnosed. New World species seem to be fairly resistant to infection. The syndrome reported most often occurs in young African Grey parrots. Recently a suspected reovirus infection has caused serious losses in budgerigars in the United Kingdom (see Supplemental Readings).
Pathologic lesions include disseminated coagulation necrosis of the liver, spleen, bone marrow, and intestinal lamina propria. Clinically, we have seen cases present with hepatitis and aplastic anemia and fairly rapid death. There are NO inclusion bodies seen with this disease.
The virus may persist in the environment. It is acquired through ingestion and inhalation. Psittacine reovirus vaccines are in the works but not yet available. Chicken reovirus vaccine is ineffective in psittacines because it represents a different serotype.
 Multifocal hepatic necrosis in a reovirus
infection
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12. Duck Viral Hepatitis
(Viral hepatitis of ducks, DVH)
Duck viral hepatitis is a peracute, enterovirus (picorna virus) disease of young, commercially raised Peking ducklings. Natural outbreaks have not been reported in other poultry breeds. In 1949, this disease was responsible for a disease outbreak that killed 750,000 ducklings on Long Island, NY where there was extensive commercial duck raising.
12.1. Clinical Signs
- Rapid onset of acute mortality which often approaches 100%.
- Affected ducklings become lethargic, squat with their eyes closed, fall to one side, show convulsion and die in opisthotonos. Death occurs within one hour after the first clinical signs are observed.
13. Duck Viral Enteritis
(Duck plague, DVE)
This is an acute, herpes virus disease of wild and domestic anseriformes (ducks, geese and swans). Wild ducks are the natural host and often transmit disease to domestic and captive breeds. There is marked variation in the susceptibility and mortality of this disease in wild duck species. Massive outbreaks are sometimes seen in waterfowl with hundreds of birds affected. Duck plague herpes virus can remain latent in the trigeminal ganglion of carrier animals similar to other herpes virus. Shedding or active disease is produced during periods of stress.
13.1. Clinical Signs
- Serous and mucoid occulonasal discharge with diarrhea and occasional CNS signs
- Anorexia, weakness and ataxia with photophobia and pasted eyelids.
- The ground where sick birds have rested is often blood-stained.
- Penile prolapse
13.2. Diagnosis
- Hemorrhages in liver, pancreas, intestinal mucosa, lungs and kidneys are the typical gross lesions.
- Hemorrhage into body cavities may also occur.
- The esophageal-proventricular junction often shows a localized region of mucosal hemorrhage.
- Annular bands of hemorrhage are sometimes seen in the small intestine that correspond with the GALT.
- Crusty plaques are sometimes found on esophageal, cecal and rectal mucosa.
- Intranuclear, eosinophilic inclusions typical of herpes virus disease can usually be found associated with necrotic foci in the liver and mucosal epithelial cells.
- Vasculitis is also a common microscopic lesion.
Fowl cholera is an important differential diagnosis to consider in an outbreak of duck plague. A Gram stain of peripheral blood from a bird infected with P. multocida will always show many bipolar, gram negative rods.
14. Proventricular Dilatation Syndrome (PDD)
It has been suggested that Psittacine proventricular dilatation syndrome, also known as lymphoplasmacytic ganglioneuritis and encephalomyelitis, neuropathic gastric dilatation, and "Macaw Wasting disease" (described in the 1980's) is a viral induced syndrome. Very recent evidence points to a strain of paramyxovirus (aPMV-1) as the causative agent, but other viruses have also been suggested.
This disease is classically seen in Macaws, but has more recently been consistently reported in cockatoos, conures, amazons, african greys, etc. In the last 10 years it has been described in over 50 different species including sporadic reports in some non-psittacine wild birds. It is eventually 100% fatal.
14.1. Clinical signs
Clinical signs include weight loss, maldigestion, and regurgitation. CNS signs may develop in very late stages of the disease.
14.2. Diagnosis
Radiographs usually demonstrate a grossly dilated proventriculus with or without contrast upper GI radiography. 30% of cases can be diagnosed with a crop biopsy, showing characteristic lesions. Other cases can only be positively diagnosed with a full thickness proventricular biopsy. Histology shows lymphocytic myenteric ganglioneuritis in the walls of the proventriculus, ventriculus and sometimes the rest of the GI tract. Leiomyositis, smooth muscle degeneration, and sometimes nonsuppurative encephalomyelitis may also be identified at necropsy.
Rule-outs for a dilated proventriculus include infectious problem (incl. fungal gastritis), heavy metals toxicosis, and gastric foreign body obstruction.
14.3. Treatment
There is no specific treatment other than management of the chronically ill patient, supportive care for malnutrition/maldigestion and weight loss. this disease is uniformly fatal.
| REMEMBER other viruses also involving the gastrointestinal system: |
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15. Eastern Encephalitis (commonly known as Eastern Equine Encephalitis) and other Togavirus diseases of birds.
Disease susceptibility to Eastern and Western encephalitis virus among different species of birds is striking. These viruses are transmitted by mosquitoes between many wild birds. Most avian species do not develop clinically apparent disease although seroconversion is common. A few species such as ring-necked pheasants, chukkar partridge, cardinals and sparrows are susceptible to infection with a resulting high mortality. Many of these species are not indigenous to the Eastern US. Domestic turkeys, ducks and pigeons are also susceptible but in these species death usually seen only in younger birds. The chicken seldom develops clinical disease but this is due to insufficient exposure to appropriate mosquito vectors. Chickens are susceptible to lethal infection with EE virus but natural disease is uncommon in chickens because of the low frequency of exposure to C. melanura in and around near chicken houses. C. pipiens the mosquito species commonly found in these areas and these species is a poor transmitter of the EE virus.
15.1. Atypical viscerotropic EE
A severe, peracute disease has been seen in captive emus in the US. Clinical signs consist of recumbency, regurgitation, and profuse, bloody diarrhea. Death is rapid, usually after one day of illness. Gross lesions consist of blood-stained feathers around the vent. The intestinal lumen is filled with variable amounts of blood and mucus. Some of the birds show patchy, subcapsular hemorrhage in the liver in addition to ecchymoses on the epicardial and endocardial surfaces. Splenomegaly and hemoperitoneum is also present. Severe, diffuse, necrotizing hepatitis with necrotizing splenitis and splenic vasculitis are the principle microscopic finding. Microscopic brain lesions are not present! Infection may be transmissible directly between birds without mosquito vectors.
Viscerotropic EE virus infection has been infrequently reported in wild cranes.
Vaccination of ratite species with the killed equine product has now become common but a recent report of mortality in a sand hill crane and a palm cockatoo previously vaccinated for EE has been reported. Recent evidence shows that vaccination in emus does protect against a lethal challenge, showing active increase in titers.
16. 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 http://www.nwhc.usgs.gov/research/west_nile/west_nile.html .
16.1. 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.
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).
17. Avian Encephalomyelitis
(Epidemic tremor, AE)
Baby chicks, usually under three weeks of age are most often infected with this picorna virus. Young turkeys, pheasants and Coturnix quail can also be naturally infected. AE should be considered the avian counterpart of Teschen Disease in Swine, Polio in humans and Mouse Polio in laboratory mice.
17.1. Clinical Signs
- Unsteadiness, paresis and fine muscle tremors.
- Variable mortality - up to 60%
- Older birds are usually asymptomatic.
17.2. Diagnosis
Microscopically, diffuse nonsuppurative encephalitis with central chromatolysis of neurons is evident. The nucleus rotundus and nucleus ovidalis are especially useful to examine. Dense lymphocytic aggregates are found in gizzard, proventriculus and pancreas. Although these are best appreciated on microscopic examination, they can sometimes be observed at the gross level as pale streaks in the musculature. On the basis of clinical history and microscopic lesions the disease can usually be differentiated from Newcastle Disease and the neural form of Marek's Disease.
| REMEMBER other viruses also involving the central nervous system: |
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18. Avian pox
(Fowl pox, Wet pox) Avian pox is a widespread disease infecting many wild and domestic avian species. Most birds are susceptible to species specific poxviruses. All of the avian poxviruses are antigenically related. All pox viruses persist for a long time in the environment.
18.1. Fowl Pox
18.1.1. Clinical Signs
- Slow spreading with indolent clinical course.
- Birds with fowl pox behave normally other than showing cutaneous lesions.
- Lesions typically appear on non-feathered parts of the body: comb, wattles, shanks and feet.
- In wet pox, opaque plaques or nodules form on mucus membranes of the mouth, esophagus and trachea. This may result in death secondary to anorexia.
18.1.2. Diagnosis
Microscopic skin lesions are proliferative with swelling and hydropic changes of the epithelial layer. Intracytoplasmic, eosinophilic inclusions (Bollinger bodies) are apparent on microscopic examination. Fowl pox inclusions will stain positively with histologic stains used for lipids (Sudan IV, Oil red 0: this characteristic is only seen with avian poxviruses).
18.2. Psittacine Pox
Psittacine pox has been seen most often in young imported Blue front Amazon parrots. It is also seen in other amazons, lovebirds, macaws, Pionus parrots, budgies, lories, etc. There is both a cutaneou
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