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Chlamydophila psittaci

Avian Chlamydiosis

Etiology

The etiologic agent of avian chlamydiosis [psitacosis] is Chlamydophila psittaci, an obligate, intracellular, gram negative bacteria. Chlamydophila psittaci includes 8 known serotypes, 6 of which naturally infect birds. Each serotype appears to have a predilection for infecting a different group or order of birds. Some serotypes are endemic to specific populations of wild birds. In domestic fowl, C. psittaci has been categorized into 2 general categories: highly virulent strains (those that cause acute epidemics with a 5-30% mortality rate) and less virulent strains (those that cause slowly progressive epidemics with mortality rates typically under 5%).

Host range

Chlamydophila psittaci is capable of causing clinical disease in hundreds of species of birds, both domestic and wild. However, there is a wide species variation in terms of disease susceptibility. Chickens are relatively resistant to C. psittaci, while the infection is often severe in ducks and geese. Pigeons, turkeys, pheasants, quail, and partridges are all susceptible to various degrees. The disease can also be debilitating in parrots and other psittacine cage-birds.

C. psittaci poses a significant public health concern for humans. Outbreaks in humans usually occur following exposure in poultry processing plants. Infections can also result from handling infected birds and inhaling the bacteria. The severity of human infection can range from asymptomatic to severe pneumonia. Appropriate precautions should always be taken when handling any bird suspected of possible avian chlamydiosis infection.

Epidemiology

Chlamydophila psittaci is primarily transmitted by inhalation and ingestion of contaminated materials (e.g. fecal dust and respiratory exudate). The elementary body stage of Chlamydophila psittaci is highly resistant to drying and may persist in the environment for many months.

The incubation period varies depending on the dose and pathogenicity of the strain. In highly virulent strains, incubation may be 2-8 weeks. Morbidity is often 50-80% and mortality ranges from 10-30%. In low virulence strains, incubation may be as short as 5-10 days and morbidity is usually 1-4%.

Chlamydophila psittaci is distributed worldwide. Wild birds are considered natural reservoirs for the infection, many of which are chronically, but asymptomatically, infected and only shed the organism under physiologically stressful conditions.

Epidemics of Chlamydophila psittaci vary greatly by avian species. Outbreaks in turkeys tend to be explosive, involving one or more flocks with high mortality. Outbreaks in ducks vary by geographic region. In the United States, Chlamydophila psittaci has not been a significant problem in ducks however, in Europe there have been a number of recent outbreaks.

Clinical Signs

Clinical signs are variable and depend on host species, age, and strain of Chlamydia. Some birds may be completely asymptomatic. Affected birds may show fever, drop in feed consumption, lethargy, drop in egg production (initially 10-20% but may cease totally), diarrhea (yellow-green and gelatinous), oculonasal discharge, and respiratory signs. The more virulent the strain, the more severe these signs generally become.

Watery diarrhea and neurologic abnormalities such as trembling, ataxia, and paralysis have been noted in ducks, geese, and pigeons. Unilateral or bilateral conjunctivitis with purulent discharge often occurs. Ducks are particularly susceptible and may become emaciated and die in convulsions.

Post-mortem Lesions

On post-mortem examination, in virulent strains, findings may include diffuse pulmonary congestion and the accumulation of fibrinous exudate in the pleural cavity. The pericardial membrane may be congested, thickened, and have fibrinous exudate on its surface. The Heart may be enlarged and its surface covered with fibrin plaques and dry yellow exudate. The liver may be enlarged, discolored, and coated with fibrin. Air sacs are often thickened and coated with fibrin. The spleen may be enlarged, dark, and friable with small pinpoint white lesions, caused by focal cellular proliferation. The serosal surfaces of all the organs of the coelomic cavity may have vascular congestion and white fibrinous exudate. In severe cases, a dark red transudate may be found in coelomic cavity.

Differential Diagnosis

Chlamydiosis in turkeys must be differentiated from Mycoplasma gallisepticum, avian influenza, aspergillosis, and fowl cholera. Lesions in turkeys closely resemble those of M. gallisepticum. In ducks, chlamydiosis must be differentiated from duck viral hepatitis and duck septicemia.

Diagnosis

Chlamydophila psittaci organisms can often be identified on impression smears taken from affected tissues stained by the Giemsa or Gimenez methods. Intracytoplasmic inclusions are helpful, but confirmation requires demonstration of causal organisms. A definitive diagnosis is usually obtained by isolation and identification of chlamydia organisms or by demonstration of a four-fold rise in antibody titer to chlamydia group antigen. Antigen detection methods include immunohistochemistry (immunofluorescent assay or immunoperoxidase) and enzyme-linked immunosorbent assay (ELISA). Serologic methods include direct complement-fixation, latex agglutination, gel diffusion, and direct and competitive ELISA.

Prevention and Control

Commercial vaccines against Chlamydia are not available. The immune response necessary to elicit complete protection against challenge is very complex and is probably driven by cellular immune mechanisms. Broad spectrum antibiotics in the feed like chlortetracycline (CTC) are commonly used to treat infections in poultry and pet birds.

Selected References

  1. Andersen, A.A. and D. Vanrompay. 2008. Avian Chlamydiosis (Psittacosis, Ornithosis). In Diseases of Poultry, 12th ed. Y.M. Saif. et al. (ed.). Blackwell Publishing, Ames, Iowa.
  2. Andersen, A.A. and D. Vanrompay. 2008. Chlamydiosis. In A Laboratory Manual for the Isolation and Identification of Avian Pathogens, 5th edition. L. Dufour-Zavala Louise et al. (ed.) OmniPress, Inc., Madison, Wisconsin.
  3. Andersen, A.A. and D. Vanrompay. 2000. Avian chlamydiosis. Rev Sci Tech 2:396-404. Review.
  4. Charlton, B. R. (ed). 2006. Avian Disease Manual, 6th ed. American Association of Avian Pathologists (AAAP), 953 College Station Road, Athens, Georgia 30602-4875.
  5. Eidson, M. 2002. Psittacosis/avian chlamydiosis. J Am Vet Med Assoc 221(12):1710-2. Review.
  6. World Organization for Animal Health (OIE) website. 2008. www.oie.int

Thank you to the following individuals for reviewing these materials:

Jaime Ruiz
Charles Hofacre
Jose Bruzual

Differentials: 
Aspergillus
Avian Influenza
Duck Septicemia
Duck Viral Hepatitis
Mycoplasma gallisepticum
Fowl Cholera