Psittacosis (Due to Chlamydia psittaci)

Reviewed for currency January 14, 2021

Epidemiology

Chlamydia psittaci is common in birds (often as asymptomatic carriers) and domestic animals. Infection is therefore a hazard to pet owners, pet shop employees, poultry farmers (turkey-associated psittacosis has the highest attack rate in psittacosis epidemics), workers in abattoirs and processing plants (psittacosis is the most common abattoir-associated pneumonia), and veterinarians. However, anyone in contact with an infected bird or animal is at risk. Human cases occur both sporadically and in outbreaks.

Most patients with psittacosis have had some contact with a bird, usually as a pet. In fact, the importation of exotic birds (sometimes illegally) has been correlated with an increase in human psittacosis in the United States, Sweden, England, and Wales. Often, the bird was recently acquired or was ill. Bird contact may achieve surprising levels of intimacy. Patients have acquired psittacosis by kissing their parrot or by performing mouth-to-mouth resuscitation on a dying bird. Other patients have had more trivial or transient exposure, such as visits to public bird parks, transporting pigeons by car, passing through a room in which infected birds were sitting, sharing a stage with a parrot, or guarding crates of pigeons at a railroad depot. Still, some patients (25%) have had no avian exposure, and other animal sources may rarely be implicated, as in a recent outbreak in a veterinary school following exposure to equine fetal membranes.

Birds transmit the infection to their nestlings, which in turn shed the organism during periods of both illness and good health. In bird populations studied, there is a baseline prevalence of 5% to 8% of C. psittaci carriage. This may increase to 100% when birds are subjected to the stress of shipping, crowding, and breeding.

It is likely that all birds are susceptible. More than 130 avian species have been documented as hosts of C. psittaci. These include members of the parrot family (macaws, cockatoos, parakeets, budgerigars), finches (canaries, bullfinches, goldfinches, sparrows), poultry (hens, ducks, geese, turkeys), pigeons, pheasants, egrets, seagulls, and puffins.

Infection may appear in birds years after exposure. Infected birds may be asymptomatic or obviously sick. In the latter case, birds may exhibit shivering, depression, anorexia, emaciation, dyspnea, and diarrhea, frequently with closed eyes and ruffled feathers. Spontaneous relapse and remittance of the illness may occur, although it is during periods of illness that infected birds excrete the largest numbers of organisms. Discharge from their beaks, eyes, feces, and urine is infective; their feathers and the dust around their cage become contaminated.

The infection is generally spread by the respiratory route, by direct contact or aerosolization of infective discharges or dust. Rarely, the bird may spread the infection by a bite. If untreated, 10% of infected birds become chronic asymptomatic carriers.

Strains from turkeys and psittacine birds are the most virulent for humans. Although most human exposure comes from avian strains of C. psittaci, disease has occurred in ranchers after exposure to infected tissues from parturient cows, goats, and sheep. Endocarditis has been attributed to avian and nonavian strains, and cats have spread feline pneumonitis to humans and other mammals. The growing practice of pet-associated therapy in nursing homes has produced a new epidemiologic risk for psittacosis.

Human-to-human and nosocomial transmissions are rare, and it is therefore thought unnecessary to isolate patients in the hospital or to give antibiotic prophylaxis to contacts. However, cases acquired from humans tend to be more severe than avian-acquired disease. Environmental sanitation is important because the organism is resistant to drying and can remain viable for months at room temperature.

Clinical Manifestations and Differential Diagnostic Considerations

The disease begins after an incubation period of 5 to 15 days. Onset may be insidious or abrupt, and the clinical manifestations tend to be nonspecific. Several syndromes may result. The infection may be subclinical, or it may resemble a nonspecific viral illness with fever and malaise or a mononucleosis-like syndrome with fever, pharyngitis, hepatosplenomegaly, and adenopathy. A typhoidal form manifests as fever, bradycardia, malaise, and splenomegaly. However, the presentation most suggestive of the cause is atypical pneumonia, with nonproductive cough, fever, headache, and chest film abnormalities more dramatic than would be suggested by the physical findings. The illness ranges in severity from an inapparent or mild disease to a fatal systemic illness with prominent respiratory symptoms.

Because many patients have an illness with nonspecific findings, the list of initial diagnoses for which patients have been referred to hospitals is extensive. This list reflects the various organ systems that may be involved in C. psittaci infection and includes the diagnoses of meningitis, tonsillitis, pneumonia, pulmonary embolism, myocardial infarction, gastroenteritis, hepatitis, peritonitis, pancreatic carcinoma, urinary tract infection, endocarditis, vasculitis, septicemia, malaria, brucellosis, fever of unknown origin, and polymyositis.

The list of considerations in the differential diagnosis is extensive, and the diagnostic possibilities depend on the presentation. A typhoidal picture suggests the mononucleosis syndrome, typhoid fever, brucellosis, tularemia, influenza, malaria, or subacute bacterial endocarditis. Respiratory signs and symptoms plus headache and myalgias should orient the clinician to causes of atypical pneumonia, such as viral pneumonia, Q fever, legionellosis, and infection with mycoplasma and C. pneumoniae. Helpful clues to a diagnosis of psittacosis, when present, are relative bradycardia, rash, hemoptysis, epistaxis, and splenomegaly.

The most common sign is fever, occurring in 50% to 100% of patients. Cough has been reported in 50% to 100%, but often it appears late in the illness and is not present initially. Headache, myalgias, and chills are reported in 30% to 70% of patients. The nonspecificity of these signs and symptoms may be puzzling until cough supervenes. Even then, the long list of other signs and symptoms that occur in fewer than half the patients may be particularly confusing due to the lack of specificity: diaphoresis, photophobia, tinnitus, ataxia, deafness, anorexia, nausea and vomiting, abdominal pain, diarrhea, constipation, sore throat, dyspnea, hemoptysis, epistaxis, arthralgia, and rash. Chest soreness is reported, but true pleuritic pain is rare.

The signs most frequently reported are fever, pharyngeal erythema, rales or other abnormalities on chest auscultation, and hepatomegaly. These occur in more than half of cases. Fewer than 50% of patients show the signs of somnolence, confusion, tachycardia, relative bradycardia, pleural rub, splenomegaly (this occurs toward the end of the first week and is helpful diagnostically), adenopathy, palatal petechiae, herpes labialis, Horder spots (see later), and muscle tenderness.

Specific end-organ involvement reflects the systemic nature of psittacosis. The organ most commonly involved in humans is the lung. This is manifested clinically by cough, dyspnea, and a variety of nonspecific auscultatory findings on physical examination. On occasion, the pneumonitis may progress to acute respiratory distress syndrome. Cardiac manifestations include pericarditis (rarely with effusion and tamponade), myocarditis, idiopathic dilated cardiomyopathy, and “culture-negative” endocarditis. Chlamydia psittaci endocarditis is associated with preexisting heart disease and may cause valvular destruction. Arterial embolism to major vessels occurs rarely. The source of these emboli and the mechanism are unknown; some are attributed to endocarditis or mural thrombi.

Hepatitis may develop, sometimes with jaundice. Anemia may result from hemolysis (both Coombs test positivity and cold agglutinins are reported) and from a reactive hemophagocytosis, in which case pancytopenia may be present. Disseminated intravascular coagulation (DIC) also complicates psittacosis. Reactive arthritis occurs 1 to 4 weeks after the initial illness; although most of the described cases are polyarticular, monarticular arthritis has also been described.

Neurologic abnormalities include cranial nerve palsy (including sensorineural hearing loss), cerebellar involvement, transverse myelitis, confusion, meningitis, encephalitis, transient focal neurologic signs, and seizures. Results of cerebrospinal fluid examination on lumbar puncture are usually normal; a small number of white cells (predominantly lymphocytes) may be seen, and the protein level on occasion is greatly elevated.

Dermatologic phenomena include Horder spots, which are a pink, blanching, maculopapular eruption on the face or trunk resembling the rose spots of typhoid fever. Also described are erythema multiforme, erythema marginatum, erythema nodosum, and urticaria, as well as acrocyanosis, subungual splinter hemorrhages, and superficial venous thromboses. Acute glomerulonephritis, acute tubulointerstitial nephritis, and acute tubular necrosis have been reported. Psittacosis has severe consequences in pregnancy and often causes DIC, hepatic dysfunction, and placentitis, with fetal compromise. Additional clinical complications of psittacosis include phlebitis, pancreatitis, and thyroiditis. Bacteremia has been demonstrated in a patient with a sarcoid-like illness.

Recent observations have suggested that C. psittaci is associated with ocular adnexal lymphomas involving orbital soft tissue, lacrimal glands, and conjunctiva. Chlamydia psittaci has been detected in lymphoma biopsies by polymerase chain reaction (PCR) assay, and tumors in some patients have regressed after treatment with doxycycline. However, the prevalence of C. psittaci in these lymphomas varies, particularly geographically, and some tumors with no evidence of C. psittaci have also responded to doxycycline therapy, suggesting that C. psittaci detection methods are inadequate or that other doxycycline-responsive organisms may cause this malignancy, or that the presumed lymphoma may not be a true malignancy but a hyperproliferative response to an infecting agent.

In addition to ocular adnexal lymphomas, C. psittaci has recently been associated with nongastrointestinal mucosa–associated lymphoid tissue lymphomas and autoimmune precursor lesions (Hashimoto thyroiditis and Sjögren syndrome).

There is no documented protection after infection, and second infections have been seen in spite of elevated levels of complement-fixing (CF) antibodies. Treated birds can also be reinfected.