Psittacosis is a rare infection caused by Chlamydophila psittaci (aka Chlamydia psittaci). The term psittacosis comes from the Greek word psittakos, meaning “parrot.” However, the infection can be acquired from many types of birds including canaries, parakeets, turkeys, pigeons, ducks and doves.1
Not all strains of C. psittaci infect humans. Some only infect cows, sheep and goats. The organism is most commonly found in wild birds.2 Humans tend to be infected most commonly after exposure to parrots, cockatiels, parakeets and macaws.3 Psittacosis is classified as an occupational disease because it is most common in zookeepers, pet shop employees, poultry farmers and ranchers. The infection is very rarely transmitted from human to human.
History of Infection
Psittacosis was first described as a human disease in Europe nearly 130 years ago. In the United States, the first pandemic occurred between 1929 and 1930. This North American outbreak was traced back to parrots imported for the 1929 Christmas trade. The frightening pandemic led to the first legal ban of bird importation in the U.S. In the years following, more laws for importation of birds were established and modified. In the U.S., all imported birds must undergo quarantine in facilities owned or governed by the U.S. Department of Agriculture. The laws continue to be revised as more is learned about psittacosis and birds.
Psittacosis is a rare cause of pneumonia; fewer than several hundred infections are reported each year. However, experts believe that these numbers are a gross underestimate of actual cases because many infections are asymptomatic and never diagnosed. In addition, empirical treatment of lung infections without identification of the organism is another reason for underreporting of the disorder.1,4 Psittacosis is a global infection but appears to be more common in countries that export birds (e.g., Brazil, Indonesia).5,6
C. psittaci is an occupational health hazard for people employed in the breeding, importation, transportation, marketing and care of pet birds. Humans often acquire the infection by handling sick birds. In addition, C. psittaci has been known to cause sporadic epidemics in turkey flocks and in poultry-processing plant workers; customs officers who have brief contact with tropical birds being smuggled into the country are also at great risk for acquiring psittacosis.7, 8In addition, casual visitors to pet shops have also been reported as having acquired the infection from sick birds.5
In the past, it was widely believed that only people who handled birds were prone to the disease; however, there are also isolated reports of acquiring the infection after mouth-to-beak resuscitation and handling feathers of infected birds. Even very brief exposures to infected birds can lead to symptomatic infection. Some infected birds may appear physically healthy and still shed the organism intermittently. Shedding of infectious particles may be activated by stress factors such as shipping, relocation, rough handling, crowding, breeding and chilling.
Birds at high risk for infections include those kept in pet stores, breeding facilities and in homes with multiple birds. These risks are amplified if a new tropical bird is introduced without following proper quarantine measures. These birds often shed the organism and infect other birds in the household.9 Birds susceptible to infections include cockatiels, macaws and parrots (particularly those from the Amazon). Young birds that are moved to new homes or given a poor diet also appear to be prime targets for C. psittaci.
Pathophysiology and Structure
C. psittaci is present in the nasal secretions and feces of infected birds. The respiratory tract is the main route of entry. Infection occurs by inhalation of organisms from infected birds or their droppings. Person-to-person transmission is rare. Once in the lungs, the organisms enter the blood and are transported to the liver and spleen. The bacteria replicate at these sites, where they cause isolated areas of necrosis. Hematogenous seeding of the lungs and other organs soon follows. The lymphocytic inflammatory response in the alveoli and interstitial spaces then leads to edema, infiltration of macrophages, necrosis and possible hemorrhage. Mucus plugs may develop in the alveoli, resulting in cyanosis and anoxia.
The host defense mechanisms against C. psittaci usually involve both cell-mediated and T-cell-dependent humoral antibody responses. Humans do not develop prolonged immunity to the organism; relapses are often reported even in patients with high antibody titers against Chlamydia.1,10
Members of the Chlamydiaceae family are small intracellular parasites and were considered to be viruses. However, they contain DNA, RNA and ribosomes, and because they make their own proteins and nucleic acids, they are now considered to be true bacteria. They have an inner and outer membrane similar to gram-negative bacteria and a lipopolysaccharide, but they do not possess a peptidoglycan layer.11 Although they synthesize most of their metabolic intermediates, they are not able to make their own ATP; thus, they are energy parasites.
Chlamydia have infectious and noninfectious forms — elementary bodies and reticulate bodies, respectively.
EBs are small and posses a rigid outside membrane supported by disulfide bonds. This membrane protects against conditions outside of a eukaryotic host cell. EBs bind to receptors on host cells and initiate infection.
RBs are the noninfectious intracellular form of chlamydia; they are its active replicating form. They possess a weak membrane lacking the disulfide bonds characteristic of the EB.
EBs bind to receptors of susceptible cell types and are internalized through endocytosis and/or phagocytosis. Once inside the host cell endosome
, EBs reorganize and become RBs. The entire intracellular life cycle of chlamydia occurs within the endosome. RBs replicate by binary fission and reorganize into EBs. The resulting inclusions may contain 100 to 500 progeny.11
Eventually, the cells and inclusions lyse (C. psittaci
) or the inclusions are extruded by reverse endocytosis (C. trachomatis
and C. pneumoniae
Figure 1: Developmental Cycle of C. psittaci
Diagram by C. Swift
Psittacosis can affect both sexes and has no age predilection; infection can occur in all age groups, including children. In the past, the mortality rate from psittacosis was almost 20%, but this was at a time when there were no effective antibiotics. Since the advent of macrolides and tetracyclines, mortality is less than 1%.