Aetiology

Infection is caused by Chlamydia psittaci, an obligate, intracellular, gram-negative bacterium.[1] Contact with birds, for example among pet bird owners, people who work in zoos or pet shops, veterinarians, poultry and wildlife workers, and diagnostic laboratorians, appears to be the primary risk factor for infection.[13] Human infection can also result from indirect environmental exposure.[13]

The association of C psittaci infection in humans exposed to birds and mammals has been known since the 1870s.[14] However, approximately 25% of affected patients deny exposure, which points to a lack of recognition of contact with an asymptomatic, but infected, bird or mammal.[13]

Most infections are acquired from exposure to psittacine (parrot-type) birds, especially budgerigars and cockatiels. However, transmission has also been documented from nonpsittacine birds, most commonly pigeons and doves, as well as poultry, free-range birds, birds of prey, ducks, and shore birds.[13][15]

Occupational exposure to commercially bred turkeys, other fowl, and mammals, or to infected tissue, can precipitate outbreaks of psittacosis.[6] Outbreaks have been observed on duck, turkey, and other poultry farms, among abattoir workers, and from exposure to feral pigeons.[1][5][6][16][17][18][19][20][21][22] There have also been reports of outbreaks associated with bird shows and in veterinary teaching hospitals.[23][24][25] Certain strains that infect poultry and psittacine birds tend to be more virulent.[1][6]

Human-to-human transmission is thought to be rare and can cause more severe disease.[5][26][27]

Pathophysiology

C psittaci has a distinct biphasic developmental cycle consisting of the infectious elementary body (EB) and the replicative form termed the reticulate body (RB). The EB attaches to the host cell and is either endophagocytosed or taken up by receptor-mediated processes that are not well understood. Once inside the cell, the organism becomes incased in an inclusion body, where there is ineffective lysosomal fusion, thus ensuring the survival of the inclusion body. The organism produces proteins that contribute to the membrane of the inclusion body. The EB transforms into an RB, which replicates by binary fission, producing intermediate bodies, where the chromatin condenses to become an EB. The EBs are released from the host cell either by cell lysis or by exocytosis of the inclusion body, leaving the cell intact, and can then infect adjacent cells. This occurs at 36 to 48 hours following infection.[28]

C psittaci can be readily cultured in permissive cell lines, including HEp-2 and buffalo green monkey cells, but great caution must be taken because of the ease of creating aerosolised particles.[Figure caption and citation for the preceding image starts]: Chlamydia psittaci-infected HEp-2 cells stained with a fluorescein isothiocyanate-conjugated monoclonal antibody against the lipopolysaccharide of Chlamydia (1000X)From the collection of Professor Deborah Dean; used with permission [Citation ends].com.bmj.content.model.Caption@1f46f275

Transmission of infection is by aerosolised particles or direct contact with faeces, nasal secretions, plumage, or tissue. There are 8 known genotypes, and likely more, of the organism; all can be transmitted to humans.[13][12] The incubation period is 5 to 14 days.[13]

The long developmental cycle and the ability of the organism to persist are likely to contribute to chronic infection, more widespread pulmonary or systemic disease, and failure of antibiotic treatment regimens. Certain strains are also considered more virulent. Consequently, a longer course of antibiotics is required for successful treatment, although some patients may still harbour persistent infection. There are reports of some resistance to azithromycin.[29]

The extent of relapse and persistent infections is unknown due to the lack of epidemiological studies and sensitive and specific tests to assess infection.

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