Avian chlamydiosis can be an inapparent subclinical infection or acute, subacute, or chronic disease of wild and domestic birds characterized by respiratory, digestive, or systemic infection. Infections occur worldwide and have been identified in at least 460 avian species, particularly caged birds (primarily psittacines), colonial nesting birds (eg, egrets, herons), ratites, raptors, and poultry. Among poultry, turkeys, ducks, and pigeons are most often affected; infection of chickens is infrequent. The disease is a significant cause of economic loss and human exposure in many parts of the world. Longterm inapparent infections lasting for months to years commonly occur and are considered the normal chlamydia-host relationship; 10–30% of surveyed avian populations may be found positive by serology. The same strain may cause mild disease or asymptomatic infection in one species, but severe or fatal disease in another species.
Etiology and Epidemiology
In 1999, the causative organism was renamed Chlamydophila psittaci but the name of the disease resulting from infection with C psittaci remains avian chlamydiosis. C psittaci is an obligate intracellular bacterium. All strains of chlamydia share an identical genus-specific antigen in their lipopolysaccharide but often differ in the composition of other cell-wall antigens, providing a basis for serotypic identification. Currently, 8 serotypes are recognized; of these, 6 (A–F), infect avian species and are distinct from mammalian Chlamydophila serotypes. Each avian serotype tends to be associated with certain types of birds (see Avian Chlamydiosis: Associations Between Avian Serotypes of C psittaci and Types of Birds). Serotype D is highly virulent for turkeys and can cause mortality of 30% or higher. Serotypes B and E are most frequently recovered from wild birds. Avian serotypes are capable of infecting people and other mammals.
Respiratory discharge or feces from infected birds contain elementary bodies that are resistant to drying and can remain infective for several months when protected by organic debris (eg, litter and feces). Airborne particles and dust spread the organism. After inhalation or ingestion, elementary bodies attach to mucosal epithelial cells and are internalized by endocytosis. Elementary bodies within endosomes in the cell cytoplasm inhibit phagolysosome formation and differentiate into metabolically active, noninfectious reticulate bodies that divide and multiply by binary fission, eventually forming numerous infectious, metabolically inactive elementary bodies. Newly formed elementary bodies are released from the host cell by lysis. The incubation period is typically 3–10 days but may be up to 2 mo in older birds or following low exposure. Host and microbial factors, route and intensity of exposure, and treatment determine clinical course.
Possible sources of C psittaci include infected birds, asymptomatic carriers, vertical transmission from infected hens, infected mammals, and contaminated environment. Stressors (eg. transport, crowding, breeding, cold or wet weather, dietary change, or reduced food availability) and concurrent infections, especially those causing immunosuppression, can initiate shedding in latently infected birds and may cause recurrence of clinical disease. Carriers often shed the organism intermittently for extended periods. Persistence of C psittaci in the nasal glands of chronically infected birds may be an important source of organisms.
Clinical Findings and Lesions
Severity of clinical signs and lesions depends on the virulence of the organism and susceptibility of the bird; asymptomatic infections are common. Nasal and ocular discharge, conjunctivitis, sinusitis, green to yellow-green droppings, fever, inactivity, ruffled feathers, weakness, inappetence, and weight loss can be seen in clinically affected birds. Clinical pathology test results vary with the organs most affected and the severity of the disease. Hematologic changes most often present are anemia and leukocytosis with heterophilia and monocytosis. Plasma bile acids, AST, lactate dehydrogenase, and uric acid elevation may be present. A radiograph or a laparoscopy may reveal an enlarged liver and spleen and thickened airsacs. Necropsy findings in acute infections include serofibrinous polyserositis (airsacculitis, pericarditis, perihepatitis, peritonitis), pneumonia, hepatomegaly, and splenomegaly. Multiple pale foci and/or petechial hemorrhages can be seen in the liver and spleen. Similar lesions are seen in other systemic bacterial infections and are not specific for avian chlamydiosis. Multifocal necrosis in the liver and spleen is associated with small granular, basophilic intracytoplasmic bacterial inclusions in multiple cell types; occasional heterophils; and increased mononuclear cells (macrophages, lymphocytes, plasma cells) in hepatic sinu-soids and splenic sinuses. Necrosis results from direct cell lysis or vascular damage. The latter is also the source of the generalized serofibrinous exudate. In chronic infections, enlargement and discoloration of the spleen or liver may be noted. Necrosis and bacterial inclusions are not seen, but the mononuclear cell response is present in these birds. Lesions are usually absent in latently infected birds, even though C psittaci is often being shed.
Because of the variety of clinical presentations and common occurrence of latently infected carriers, no single diagnostic test can reliably determine infection. Procedures to detect the organism or antibodies are used. In general, the more acute the disease, the greater the number of infective organisms and the easier it is to make a diagnosis. When birds are acutely ill, clinical findings, including hematology, clinical chemistries, and radiology or typical gross lesions, are adequate for a tentative diagnosis.
The combination of a serologic and an antigen detection test, especially PCR or culture, is a practical diagnostic scheme to confirm chlamydiosis. In live birds, the preferred sample for bacterial culture or PCR is a single swab of the choana and cloaca. Multiple samples collected for 3–5 days are recommended for detection of intermittent shedding by asymptomatic birds.
Antibodies may or may not be detectable depending on the test used, and level and stage of infection. Interpretation of titers from single serum samples is difficult. A 4-fold increase in titers between paired acute and convalescent samples is diagnostic, and high titers in a majority of samples from several birds in a population are sufficient for a presumptive diagnosis. Serologic methods include direct and modified direct complement fixation, elementary body agglutination, antibody ELISA, and indirect immunofluorescence. The elementary body agglutination test detects IgM and is useful for determining recent infection. The complement fixation methods are more sensitive than agglutination methods. High antibody titers may persist after treatment and may complicate evaluation of subsequent tests.
Antigen detection methods include immunohistochemistry (eg, immunofluorescence, immunoperoxidase), ELISA, and PCR. ELISA kits developed for detection of Chlamydia trachomatis in humans are available commercially and are relatively inexpensive. Their exact specificity and sensitivity for detection of C psittaci is most often unknown; they appear to have good specificity but somewhat low sensitivity. These kits are most useful when birds are clinically ill. PCR is the most sensitive and specific test, but results may differ between laboratories because of the lack of standardized PCR primers and laboratory method variations. False positive results are a concern with PCR as cross contamination can occur relatively easily. The organism can also be identified in impression smears of affected tissues. Chlamydiae stain purple with Giemsa and red with Macchiavello and Gimenez stains.
Immunohistochemistry is usually more sensitive than the histochemical stains mentioned above for detecting bacteria in tissue.
Confirmation requires isolation and identification of C psittaci in chick embryos or cell cultures (BGM, L929, Vero) at a qualified laboratory. Cloacal, choanal, oropharyngeal, conjunctival, or fecal swabs from live birds or tissues (eg, liver, spleen, serosal membranes) from dead birds should be submitted. Freezing, drying, improper handling, and certain transport media can affect viability. Refrigeration; placing specimens in sealed plastic bags or other containers; using a special buffer prepared from sucrose, phosphate, and glutamase (SPG buffer); and prompt delivery of fresh specimens are preferred. The laboratory should be contacted for directions on submitting samples. Concurrent infections with other, more easily diagnosed diseases (eg, colibacillosis, pasteurellosis, herpesvirus infections, mycotic diseases) may mask chlamydial infection. Laboratory and clinical findings should be correlated. Chlamydiosis must be distinguished from other respiratory and systemic diseases of birds.
Prevention and Treatment
Chlamydiosis is a reportable disease; state and local governmental regulations should be followed wherever applicable. No effective vaccine for use in birds is available. Treatment will prevent mortality and shedding but cannot be relied on to eliminate latent infection; shedding may recur. Tetracyclines (chlortetracycline, oxytetracycline, doxycycline) are the antibiotics of choice. Drug resistance to tetracyclines is rare, but reduced sensitivity requiring higher dosages is becoming more common. Tetracyclines are bacteriostatic and only effective against actively multiplying organisms, making extended treatment times (from 2–8 wk, during which minimum-inhibitory concentrations in blood must be consistently maintained) necessary. When tetracyclines are administered orally, additional sources of dietary calcium (eg, mineral block, supplement, cuttle bone) should be reduced to minimize interference with drug absorption.
Outbreaks in poultry flocks are not common. Treating infected flocks with chlortetracycline at 400–750 g/ton for a minimum of 2 wk has effectively eliminated potential risk of infection for plant employees. The medicated feed must be replaced by nonmedicated feed for 2 days before slaughter and processing.
In companion birds, use of chlortetracycline-medicated feeds for 45 days is a standard recommendation for imported birds (see Pet Birds: Chlamydiosis) Difficulties in palatability of the feed itself or the high level of antibiotic necessary for adequate blood levels have limited its use. Doxycycline is the current drug of choice as it is better absorbed, has less affinity for calcium, better tissue distribution, and a longer half-life than other tetracyclines. Doxycycline added to feed or water can also result in adequate blood levels and has less effect on normal intestinal flora than does chlortetracycline. The dosage and duration of the treatment varies between species. Protocols derived from controlled studies performed in the particular species treated should be used when available.
A reliable parenteral treatment in psittacine species is the use of a specific IV doxycycline formulation (Vibravenos®; Pfizer) administered IM at 75–100 mg/kg every 5–7 days for 4 wk and subsequently every 5 days for 2 more weeks. This formulation is not available in the USA. Other doxycycline IV or IM formulations are not equivalent.
Long-acting oxytetracycline at 500–100 mg/kg, SC, every 2–3 days for 30 days, provides adequate continuous blood levels and results in elimination of shedding within 24 hr. However, focal necrosis at injection sites may be extensive, which limits the usefulness of this treatment. This option is best kept to initiate treatment.
Azithromycin and quinolones are effective for treating chlamydiosis in human patients but have not yet been adequately evaluated in birds. Supportive care for acutely affected birds also aids recovery.
Appropriate biosecurity practices are necessary for controlling the introduction and spread of chlamydiae in an avian population. Minimal standards include quarantine and examination of all new birds, prevention of exposure to wild birds, traffic control to minimize cross-contamination, isolation and treatment of affected and contact birds, thorough cleaning and disinfection of premises and equipment (preferably with small units managed on an all-in/all-out basis), provision of uncontaminated feed, maintenance of records on all bird movements, and continual monitoring for presence of chlamydial infection.
The organism is susceptible to heat (it may be destroyed in <5 min at 56°C) and most disinfectants (eg, 1:1,000 quaternary ammonium chloride, 1:100 bleach solution, 70% alcohol, etc), but is resistant to acid and alkali. The organism may persist for months in organic matter such as litter and nest material.
Avian chlamydiosis is a zoonotic disease that can affect people following exposure to aerosolized organisms shed from the digestive or respiratory tracts of infected live or dead birds or by direct contact with infected birds or tissues. Human disease most often results from exposure to pet psittacines and can occur even if there is only brief proximity to a single infected bird. Other persons in close contact with birds such as pigeon fanciers, veterinarians, farmers, wildlife rehabilitators, zoo keepers, and employees in slaughtering and processing plants are also at risk.
Some individuals, especially pregnant women and those with impaired immunity, are more susceptible than others. The illness in people is usually respiratory and varies from flu-like symptoms to systemic disease with pneumonia and possibly encephalitis. Precautions should be taken when examining live or dead infected birds to avoid exposure (eg, dust mask or plastic face shield, gloves, detergent disinfectant to wet feathers, and fan-exhausted examining hood).
Last full review/revision March 2012 by Arnaud J. Van Wettere, DVM, MS, DACVP