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.. The disease is a significant cause of economic loss and human exposure in many parts of the world.
Etiology and Epidemiology
Chlamydia psittaci, formerly renamed Chlamydophila 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, thus providing a basis for serotypic identification. Eight serotypes are recognized; of these, six (A–F) infect avian species and are distinct from mammalian Chlamydia serotypes. More recently, strains of C psittaci have been classified using genetic differences in the omp1 gene into nine genotypes. Seven of these (A, B, C, D, E, F, and E/B) are found in avian species and usually correspond to the equivalent serotype. Each avian serotype/genotype tends to be associated with certain types of birds (see Associations between Avian Genotypes of and Types of Birds). The same serotype/genotype may cause mild disease or asymptomatic infection in one species but severe or fatal disease in another species. Serotype A and D are highly virulent for turkeys and can cause mortality of ≥30%. Serotypes B and E are most frequently recovered from wild birds. Avian serotypes are capable of infecting people and other mammals.
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Transmission is by the fecal-oral route or by inhalation. 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 several months in older birds or after 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 environments. Stressors (eg, transport, crowding, breeding, cold or wet weather, dietary changes, or reduced food availability) and concurrent infections, especially those causing immunosuppression, can initiate shedding in latently infected birds and 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.
Long-term inapparent infections lasting for months to years are common and are considered the normal Chlamydia-host relationship. The prevalence of infection varies considerably between species and by geographic location. Infection is endemic in commercial turkey flocks; no clinical signs or mild respiratory signs and low mortality are the common presentations; outbreaks are rare. Although chickens are relatively resistant to clinical disease, asymptomatic infection is frequent. Epidemiologic studies report prevalence varying from 10% to >90% using serology, culture, or PCR detection; 3%–50% of surveyed wild avian populations may be seropositive.
Clinical Findings and Lesions
Severity of clinical signs and lesions depends on the virulence of the organism, infectious dose, stress factors, and susceptibility of the bird species; 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 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 may be increased. 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 tan to white to yellow 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 sinusoids 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 conjuctival, choanal, or cloacal swab. Multiple samples collected throughout 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 on the level and stage of infection. Interpretation of titers from single serum samples is difficult. A four-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 to determine recent infection. The complement fixation methods are more sensitive than agglutination methods. High antibody titers may persist after treatment and complicate evaluation of subsequent tests.
Antigen detection methods include immunohistochemistry (eg, immunofluorescence, immunoperoxidase), ELISA, and PCR. ELISA kits developed for detection ofChlamydia trachomatis in people 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, because cross-contamination can occur relatively easily. The organism can also be identified in impression smears of affected tissues (eg, liver, spleen, and lung). 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 embryo or cell cultures (BGM, L929, Vero) at a qualified laboratory. Cloacal, choanal, oropharyngeal, conjunctival, or fecal swabs (in a special Chlamydia transport media) from live birds, or tissues (liver and spleen preferred) from dead birds should be refrigerated and submitted promptly to the laboratory. Freezing, drying, improper handling, and improper transport media can affect viability. The laboratory should be contacted for directions to submit 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
Human and avian 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 prevents 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 effective only 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 of clinical disease in poultry flocks are not common. Treating infected flocks with chlortetracycline at 400–750 g/ton of feed for a minimum of 2 wk has effectively decreased potential risk of infection for plant employees. The medicated feed must be replaced by nonmedicated feed for 2 days before slaughter and processing. Calcium supplementation must be withheld during treatment with chlortetracycline, with calcium concentration in the feed reduced to ≤0.7%. Medicated feed should be provided for 45 days if elimination of the organism is attempted. Use of some tetracycline antibiotics and doxycycline in poultry is prohibited, and state regulations should be followed. Persistence of oxytetracycline residues in eggs of laying hens is 9 days, and persistance of doxycycline residues is 26 days after administration at 0.5 g/L for 7 days.
In pigeons and companion birds, use of chlortetracycline-medicated feeds for 45 days was historically a standard recommendation for imported birds (see 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, because 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 (see Chlamydiosis). Also see information in the Compendium of Measures To Control Chlamydophila psittaci Infection Among Humans (Psittacosis) and Pet Birds (Avian Chlamydiosis), 2010, National Association of State Public Health Veterinarians (NASPHV). When specific information is lacking, empiric starting dosage of 400 mg/liter of water, or 25–50 mg/kg/day PO, has been suggested.
Appropriate biosecurity practices are necessary to control 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. It may persist for months in organic matter such as litter and nest material, but thorough cleaning before disinfection is necessary.
Avian chlamydiosis is a zoonotic disease that can affect people after 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 contact with 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 or hatcheries are also at risk. Recent studies showed that zoonotic transmission of C psittaci in poultry industry workers is likely underestimated. Precautions should be taken when examining live or dead infected birds to avoid exposure (eg, dust mask and plastic face shield or goggles, gloves, detergent disinfectant to wet feathers, and fan-exhausted examining hood).
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 endocarditis and encephalitis.
Last full review/revision July 2013 by Arnaud J. Van Wettere, DVM, MS, PhD, DACVP