The most common avian diseases:
Psittacine Beak and Feather Disease
The virus causing this disease is a member of the Circoviridae. The molecular structure of the genome of the virus is roughly a 2,000 base, circular, single stranded DNA.
PBFD virus has a strong resemblance to Porcine Circovirus as well as to a number of plant viruses such as the Banana Bungy virus. The disease is thought to be specific for psittacines and all psittacine species should be considered susceptible. Parrots known to be particularly affected by PBFD include, but are not limited to, Cockatoos, Macaws African Grey Parrots, Ringneck parakeets, Eclectus Parrots, Lovebirds.
Causes fatal infections, primarily in young birds. Older birds may overcome the disease with few lasting affects.Some believe that these surviving birds become carriers able to shed the disease at a later date. Others believe that a percentage of birds are able to eradicate the disease from their system leaving them with a natural immunity that can be passed on to their offspring. The virus that causes PBFD can also affect the liver, brain, and immune system causing diminished resistance to infections. Consequently premature death usually occurs from these secondary bacterial, fungal, parasitic, or viral infections.
Transmission Transmission of the virus from one individual to another is primarily through direct contact, inhalation or ingestion of aerosols, crop-feeding, infected fecal material, and feather dust. The virus can also be transmitted via contaminated surfaces such as bird carriers, feeding formula, utensils, food dishes, clothing, and nesting materials. The viral particles, if not destroyed can remain viable in the environment for months, long after the infected bird is gone.
Symptoms include irreversible loss of feathers, shedding of developing feathers, development of abnormal feathers, new pinched feathers, and loss of powder down. Other possible symptoms include overgrown or abnormal beak, symmetrical lesions on the beak and occasionally nails.
Immunosuppression,rapid weight loss, and depression are also possible in later stages of the disease.
Secondary viral, fungal, bacterial or parasitic infections often occursas a result of diminished immunity caused by a PBFD viral infection. Additional symptoms not mentioned above including elevated white cell counts are generally due to secondary infections and may not be directly related to PBFD virus infections.
Prevention Strict isolation of all diseased birds to halt the the spread of the disease. DNA testing of all birds of susceptible species to rule out latent infection. DNA testing of aviary equipment and environment to test for possible contamination.
Treatment No known treatment. Experimental vaccines are being developed.
Diagnosis Skin biopsy, surgical biopsy of feather and shaft, or PCR testing of blood, swab, and feather samples. PBFD should be considered in any bird suffering from abnormal feather loss or development. A biopsy of the abnormal feathers including the calimus (shaft) of the feather can be examined for signs of virus. However, since the PBFD virus does not affect all feathers simultaneously this method of evaluating a sample may have a high degree of error. Additionally, birds with PBFD can have normal feathers and the PCR test is the most effective method available for detecting the virus in birds before feather lesions develop. Some birds infected with the virus, test positive, but never show clinical signs. Other birds which test positive may develop an immune response sufficient enough to fight off the infection and test negative after 30-90 days. Therefore, it is recommended to re-test all PBFD positive birds 60-90 days after the initial testing was completed. If the second sample remains positive, the bird should be considered permanently infected and can be expected to show clinical symptoms of the disease.
Avian Pacheco PVD
Description: Pacheco’s disease – This disease is caused by a number of closely related members of the herpesviridae. Herpesviruses are 120 to 220 nm in diameter and their genome has a double stranded DNA structure. Replication of the virus occurs in the nucleus of a cell. These viruses primarily infect lymphatic tissue (B or T cells), skin (epithelial cells) and nerve cells.
PDV was first recognized in Brazil where aviculturalists began seeing birds dying only a few days after becoming ill. The virus can start shedding in the feces and nasal discharge of an infected bird in as little as 3-7 days after infection. Considered highly contagious , PDV can spread rapidly through an aviary. Often the first sign that the disease is present is when a new bird is introduced to an aviary and healthy birds begin mysteriously dying. Pacheco’s disease is often fatal and affects psittacines of all ages. New World psittacines seem to be more susceptible to the disease than Old World psittacines.
Transmission of PDV is generally through infected feces and nasal discharge. PDV remains remarkably stable outside the host body as a dust or aerosol. This dust or aerosol contaminates the air that is then inhaled by another possible host. Contaminated surfaces, food, and drinking water may also contribute to the spread of the disease. Birds can be asymptomatic carriers of Pacheco’s virus. Some believe that any bird that has survived an outbreak of the disease should be considered as a possible carrier. PDV can be reactivated when the bird is under stress such as during breeding, loss of mate, or change and environmental changes. Once it is reactivated the virus is shed in large numbers in the feces of the infected bird.
Symptoms include lethargy, diarrhea, ruffled feathers, sinusitis, anorexia, conjunctivitis, and tremors in the neck, wing and legs.
Fecal material may become discolored with urates becoming green indicating possible liver damage has occurred. Birds generally die from massive liver necrosis characterized by an enlarged liver, spleen and kidneys. However, some birds die suddenly with no specific or observable symptoms.
Seemingly healthy birds often die quickly from Pacheco’s disease. Generally stress associated with relocation, breeding, loss of mate or climate changes can activate the virus and result in activation of the disease and it’s symptoms as well as shedding large numbers of the virus in the feces.
Prevention: Isolate all birds shedding PDV. Disinfect all contaminated surfaces with an oxidizer such as chlorine bleach (as Pacheco’s virus is resistant to many disinfectants, alcohol does not work because it is not an oxidizer). It is also important to replace all air filters and clean vents and fan blades.
A killed virus vaccine is available and can be given in a series of two injections, 4 weeks apart (yearly booster shots are required). Some species, such as cockatoos and Eclectus parrots, have had vaccination reactions such as granulomas and paralysis. Additionally, the vaccine may not protect against all forms of PDV. Only birds with high risk of exposure, such as pet store birds, should be vaccinated.
Quarantine all new birds for 30-60 days and use PCR testing to determine whether or not birds are infected. Isolate birds who have been exposed to Pacheco’s virus.
Acyclovir is effective against some strains of Pacheco’s but may cause kidney damage. Acyclovir works best when treatment is started before symptoms appear.
PCR and sequence testing for specific PDV DNA. Histopathology.
Description: Chlamydia psittaci – also referred to as Psittacosis, Parrot Fever or chlamydiosis. The word Psittacosis comes from the Greek word Psittakos, meaning parrot. Chlamydia are gram negative, spherical, (0.4-0.6 micron diameter), intracellular parasites that people sometimes referred to as “energy parasites” because they use ATP (a crucial energy containing metabolite) produced by the host cell, hence, the term “energy parasites.
Incubation periods in caged birds vary from days to weeks and longer. Most commonly this period is approximately 3 to 10 days. Latent infections are common and active disease may occur several years after exposure. The incubation period of this disease is however difficult to assess due to these chronically infected birds that develop persistent, asymptomatic infections.
In birds, C. psittaci may manifest itself as an upper respiratory infection with nasal, and or ocular discharge, diarrhea, or a combination of all three. In some cases, birds may be infected but show no signs. These cases are of concern because these birds may become carriers and shed the organism.
A major concern with C. psittaci is the zoonotic potential of the organism. A zoonotic disease is an infection which can be transmitted from animals to humans. C. psittaci is also one of the major causes of infectious abortion in sheep and cattle.
*C. psittaci is related to Chlamydia trachomatis, the most common human STD, and Chlamydia pneumonia, a cause of human pneumonia.
Transmission: Transmission of this organism from one host to another is primarily through the air. The bacteria is shed from an infected bird in the nasal and or ocular secretions, fecal material, and feather dust. The organism remains remarkably stable outside the host body and dries as a dusty substance. This dust or aerosol contaminates the air that is then inhaled by another possible host. Susceptibility as well as the amount of contamination determine whether or not the new host becomes infected with the disease. Vertical transmission through the egg has been shown in domesticated ducks.
The disease has a greater chance of spreading in overcrowded conditions, stale air environments, nest-boxes, and brooders. Pet shops, bird marts, and quarantine stations are also high risk areas.
*Transmission of the Chlamydial organism from birds to humans has been confirmed in a number of cases. Although psittacosis infection in humans is rare it is potentially dangerous for persons who are sick, elderly, immunosuppressed (e.g., HIV patients) or pregnant. These people should consult their doctor for more information concerning Chlamydia psittaci.
In young birds clinical sings can include rough plumage, low body temperature, tremor, lethargy, conjunctivitis, dyspnea, emaciation, sinusitis, yellow to greenish droppings or grayish watery droppings may also be displayed.
Adult birds may develop symptoms such as tremors, lethargy, ruffled feathers, progressive weight loss, greenish diarrhea, occasional conjunctivitis, and high levels of urates in droppings. Birds infected with Chlamydia may develop one or several of these symptoms as the disease progresses. Clinical changes associated with a Chlamydia infection include WBC elevated 2-3 times, Hct decreased 25-40%, SGOT elevated at least 2-3 times the normal levels, LDH elevated by at least 20%, and AST elevated by at least 2-3 times the normal limit. Other, more slight changes can occur in blood hematology and chemistry.
*In humans: abrupt onset of fever, chills, headache, loss of appetite, shortness of breath, malaise, myalgia, and conjunctivitis can occur as a result of a Chlamydia infection.
Preventing the organism from entering your facility is the best method of prevention. Test and quarantine all new birds before entering them in your aviary; avoid bird marts and bird fares where the disease can spread. Commonsense hygiene includes the removal of fecal material, and quality air circulation.
Treatment: Most treatments involve the use of tetracycline and its derivatives such as Vibramycin, Doxycycline, Oxytetracycline. The antibiotic can be given by intravenous or intramuscular injections. Antibiotics can also be given orally or mixed with palatable food. Treatment periods generally last about 45 days varying slightly depending on the treatment. *Calcium should be withheld because tetracycline binds to calcium. Citric acid in the bird’s drinking water can increase the levels of antibiotics in the blood.
*In humans tetracycline and its derivatives are generally an effective treatment for Chlamydia.
Fecal analysis, blood analysis, immunoflourescent testing, as well as PCR and nested PCR testing are excellent tool to help determine a Chlamydial infection.
Avian Tuberculosis (Mycobacterium avium)
Description Mycobacterium (ATB) – Straight or slightly curved, non motile rods, 0.20.6 x 1.0 µm. Although difficult to stain, rods are Gram positive. After staining with basic fuchsin, cells resist decolorization with acidicethanol and are therefore termed acidalcoholfast bacilli (AFB). This characteristic is due to the high level of lipid in mycobacterial cell walls.
There are seventyone validly named species of Mycobacterium and an additional three subspecies The principal pathogens in the genus are M. bovis, M. leprae and M. tuberculosis but, in all, thirtytwo species are known to be pathogenic to humans or animals. Species of Mycobacteria other than those above are often referred to as “atypical mycobacteria”. The most commonly encountered pathogens among the atypical mycobacteria are species of the Mycobacterium avium complex. The M. avium complex (MAC) its considered to contain M. avium, M. avium subspecies paratuberculosis, M. avium subspecies silvaticum and M. intracellulare. However, poorly identified strains which show some similarity to M. avium are also frequently, and incorrectly, allocated to the complex. There are over 20 recognized serotypes within the M. avium complex.
Most birds including parrots, parakeets, cranes, sparrows, starling, emus, waterfowl raptors and softbills, have shown susceptibly to M. avium. It is believed that favorable conditions virtually all species of birds are susceptible to avian tuberculosis. It is most prevalent where there is a high population density, such as in zoos, or collections of birds.
M. avium infections are considered to be “open” meaning infected birds consistently shed large amounts of organism into the environment.
M. avium is transmitted by ingestion and inhalation of aerosolized infectious organisms from feces. Incubation in birds is weeks to years. Oral ingestion of food and water contaminated with feces is the most common method of infection. Once ingested, the organism spreads throughout the bird’s body and is shed in large numbers in the feces. If the bacterium is inhaled, pulmonary lesions may develop. Skin invasion may occur as well. The spread via infected eggs can occur, but it is not common.
The transmission of M. avium from human to human has not been convincingly demonstrated and all infections are thought to be of environmental origin.
In some cases sudden death can occur in a bird with normal body weight and outer appearance. However, in most cases a bird with TB will develop symptoms such as progressive weight loss in spite of a good appetite, depression, diarrhea, increased thirst, and respiratory difficulty. A decreased in egg production often occurs in birds that were laying eggs. Once the disease appears, it is virtually impossible to eradicate it. Eventual death is the usual outcome
Birds with the intestinal form often present with chronic wasting disease – and Proventricular Dilatation Syndrome is often one of the suspected possible diseases. In addition to weight loss, depression, diarrhea, increased urination (polyuria), abdominal distention, lameness and difficulty in breathing may be present.
Preventing M. avium is best done by minimize stress and overcrowding; Provide proper ventilation; Prevent malnutrition with a proper diet. Controlling an M. avium outbreak in zoos, bird gardens and private aviaries can be especially difficult to eradicate. New additions to the aviary should be quarantined for a minimum of 1-2 months. Testing new additions for M. avium is also a good way to prevent possible outbreaks.
All M. avium isolates that have been tested up to now are totally resistant to the antituberculous drugs currently used in humans ATB is extremely difficult to treat, and in many cases treatment is not considered a viable option.
It is difficult and lengthy process to culture the M. avium organism in the lab. An elevated White blood cell count may be present, as well as a low red blood cell count. It is sometimes possible to find bacteria in the feces by staining procedures. This however, is not specific because other acid-fast bacteria that are not M. avium may also be present. At ABI we use two techniques for testing M. avium. PCR assays which detect the actual disease causing organism, and ELISA assays which detect specific antibodies for M. avium. PCR assays are considered to be the fastest most sensitive method for detecting M. avium while ELISA assays help determine exposure to M. avium.
Proventricular Dilation Disease PDD
PDD was first recognized in macaws by Dr. H. L. Stoddard III in 1978. The condition was initially called “macaw wasting syndrome” and is also known as “psittacine wasting syndrome ” or “neuropathic gastric dilation”. Proventricular dilatation disease can occur in any psittacine but the most common birds affected are macaws, cockatoos and conures.
PDD is caused by a virus that progressively destroys the nerve supply to the proventriculus (forestomach), ventriculus (gizzard), and portions of the small intestines. As a result of the damage, birds are unable to digest their food properly. As food stays in the digestive tract bacteria accumulates and increases the chances of infection with other organisms. In some birds with PDD, the severely dilated thin wall of the proventriculus may rupture, resulting in the movement of the food into the abdominal cavity causing severe infection which many times leads to death.
Signs suggestive of PDD include weight loss over a period of weeks to months despite a good appetite, passage of undigested food, vomiting, neurological signs, abdominal distention and impaction of the crop. All of these signs may or may not be present. Although PDD is considered to be a fatal illness, this disease can persist for months. Diagnosis of PDD is done by taking a biopsy of the proventriculus. Unfortunately these biopsies are done many times after the bird dies . In some rare cases biopsy of the crop can be done to diagnose PDD. Radiographs can reveal enlarged proventriculus in adult birds which can be highly suggestive of PDD. A contrast study can determine the time it takes for food to pass from the crop through the rest the digestive tract. Many times in birds with PDD, the contrast material is delayed and hours later the ingesta is still retained in the crop.
At the present time the mode of transmission has not been established. It has been thought that the incubation may be as long as eight years but there has been cases of acute outbreaks which suggest that there is a shorter incubation period. In some cases several birds in an aviary may show clinical signs while in other cases a single bird in a breeding pair may die, with no subsequent losses in the aviary even four or five years later. It is common for many birds exposed directly or indirectly to an affected bird to remain asymptomatic. PDD has been detected in birds as young as ten weeks of age.
There is no treatment for PDD at this time. Control and prevention of PDD will require confirmation of the cause of the disease. Exposed birds should be isolated and preferably housed in single bird families.