Psittacosis, also known as parrot fever, is an infection caused by the obligatory intracellular bacterium Chlamydia psittaci. The term psittacosis is derived from the Greek word for parrot, psittakos, and was first used by Morange in 1892.
This bacterium can infect parrots, parakeets, canaries, and other avian species (eg, turkeys, pigeons, ducks). Another term for this infection is ornithosis, which describes the infection caused by nonpsittacine birds.
The largest epidemic occurred in 1930 and affected 750-800 individuals. This epidemic led to the isolation of C psittaci in several laboratories in Europe and the United States.
Psittacosis is an occupational disease of zoo and pet-shop employees, poultry farmers, and ranchers. Human-to-human transmission is rare, but possible. These cases may cause more severe disease than avian-acquired psittacosis.
Psittacosis is probably underdiagnosed because patients with milder cases may not seek medical attention or may not be reported.[1]
The primary route for infection is through the respiratory system. Infection develops after organisms from aerosolized dried avian excreta or respiratory secretions from sick birds are inhaled. C psittaci attaches to the respiratory epithelial cells. After the initial inoculation, the organism spreads via the blood stream to the reticuloendothelial system. Subsequently, secondary bacteremia causes lung infection.
Humans may acquire disease by handling sick birds. Mouth-to-beak resuscitation has also been implicated in transmission. Transient exposure to infected birds may cause symptomatic infection, even in visitors to pet shops.
United States
Reports show up to 200 cases of psittacosis annually. From 1988-97, the US Centers for Disease Control and Prevention (CDC) received 766 reports of psittacosis, which is probably an underestimate of the actual number of cases because psittacosis is difficult to diagnose, is covered by macrolide antimicrobials (which may be used empirically for therapy of community-acquired pneumonia), and often goes reported.
From 1988-2003, 935 human cases of psittacosis were reported to the CDC.[2] From 2005-2009, 66 human cases of psittacosis were reported (mean, 13; range, 8-21) to the CDC through the Nationally Notifiable Diseases Surveillance System.[1, 3]
International
Psittacosis is found worldwide. The incidence seems to be increasing in developed countries, which is correlated to the import of exotic birds.
The mortality rate of psittacosis prior to the advent of antimicrobial treatment was approximately 15-20%. The mortality rate is less than 1% with appropriate antibiotic therapy.
Psittacosis has no observed racial predilection.
Psittacosis has no observed sexual predilection.
Psittacosis occurs in all age groups, including children. The infection is more common among individuals in the middle decades of life.
Certain strains of C psittaci infect sheep, goats, and cows and may cause chronic infection and abortion.
Wild birds such as falcons have caused disease through nasal or fecal secretions.
Mowing lawns without a grass catcher has been found to be a risk factor.
Most diseases resulted from exposure to infected pet birds, usually cockatiels, parakeets, parrots, and macaws.
With appropriate antibiotic therapy, the mortality rate of psittacosis is less than 1%.
Hypoxemia and renal failure portend a poor prognosis.
Warn pet owners and pet-shop and poultry workers to be aware of possible respiratory symptoms and fever.
For excellent patient education resources, visit eMedicineHealth's Sexual Health Center. Also, see eMedicineHealth's patient education article Chlamydia.
The incubation period of psittacosis is generally 5-14 days. The longest observed incubation time was 54 days. The predominant presentation is respiratory tract infection with constitutional symptoms. Clinical findings vary.
Constitutional
Fever (50-90%)
Chills
Malaise
Respiratory
Cough (50-90%), usually not productive
Pleuritic chest pain (rare)
Dyspnea
Sore throat and mild pharyngitis (common)
Epistaxis (common)
Gastrointestinal
Nausea and vomiting (uncommon)
Abdominal pain (uncommon)
Diarrhea (rare)
Jaundice (rare)
Neurological
Severe headache (common)
Photophobia (common)
Agitation and lethargy
Dermatological - Includes facial rash (Horder spots)
Psittacosis may range from mild insidious presentations to severe pneumonia that requires mechanical ventilation.
Respiratory
Nonspecific auscultatory findings that often underestimate clinical and radiographic findings may develop.
Patients may develop fatal pulmonary embolism and pulmonary infarction.
Pleural effusion is rare.
Cardiac
Relative bradycardia is common.
Physicians may observe pericarditis, culture-negative endocarditis, and myocarditis.
Gastrointestinal
Splenomegaly occurs in 10-70% of patients, depending on the study.
When present, this sign suggests psittacosis in patients with pneumonia.
Neurological
Patients may develop meningitis, encephalitis, seizures, and Guillain-Barré syndrome, but these are rare.
Cerebrospinal fluid (CSF) findings are usually normal.
Dermatological
Patients may develop Horder spots, which are macular rashes that resemble the rose spots observed in typhoid fever but appearing on the face.
Patients may also develop erythema multiforme and erythema nodosum.
Hematological
Patients may develop anemia secondary to hemolysis.
Disseminated intravascular coagulation may occur in patients with overwhelming infections.
Renal symptoms include acute glomerulonephritis and tubulointerstitial nephritis.
Musculoskeletal symptoms include reactive arthritis that is usually polyarticular. Rarely, rhabdomyolysis has been observed.[4]
Stages of disease progression
Flulike syndromes without radiographic abnormalities
Mild-to-moderate pneumonia
Severe pneumonia
Acute respiratory failure, sepsis, and septic shock
Psittacosis is an infectious disease caused by the obligatory intracellular bacterium C psittaci.
C psittaci is associated with psittacine birds and poultry.
Psittacosis is an occupational disease of poultry farmers, pet-shop workers, and veterinarians.
Relapses may occur.
Because psittacosis is a bacterial disease, major protective immunity is unlikely to develop after a single episode of disease. The exact risk of recurrence upon reexposure is unknown. It is reasonable to advise avoidance of infected birds.
Laboratory or laboratory-related infections are possible. These are particularly underreported for several reasons, particularly because of fear for reprisal and stigma associated with such events. In addition, it would be difficult to prove that the infection is indeed laboratory related.[5]
Potential complications of psittacosis include the following:
Acute respiratory failure
Pericarditis
Myocarditis
Culture-negative endocarditis
Renal failure (rare, only a few case reports)
Disseminated intravascular coagulation (rare)
Arterial embolism (rare, 2 case reports)
Pancreatitis
Reactive arthritis
Transverse myelitis
Meningitis or encephalitis
The following are potential laboratory findings associated with psittacosis:
Chest radiographic findings are abnormal in up to 90% of cases of psittacosis.
The most common finding is unilateral, lower-lobe dense infiltrate/consolidation. Psittacosis may present in a bilateral, nodular, miliary, or interstitial pattern.
Rarely, patients develop pleural effusion.
Chest radiograph abnormalities resolve within an average of 6 weeks (range, 3-20 wk).
Few patients with psittacosis have CSF abnormalities.
CDC criteria for C psittaci infection include the following:
Findings of psittacosis may include tracheobronchitis and interstitial pneumonitis with air-space involvement and predominant mononuclear cell infiltration. Findings may also include macrophages that contain cytoplasmic inclusion bodies (ie, Levinthal-Coles-Lillie [LCL] bodies), focal necrosis of hepatocytes along with Kupffer cell hyperplasia in the liver, and hepatic noncaseating granulomata.
Consider the diagnosis of psittacosis in patients with community-acquired pneumonia who have been exposed to birds. The mainstay of medical care is antibiotic therapy.
Standard infection-control practices and droplet transmission precautions are sufficient for the medical management of humans with psittacosis, and specific isolation procedures (eg, private room, negative-pressure air flow, masks) are not indicated.[1, 6]
Notify public health authorities about cases of psittacosis.
Obtain a consultation with an infectious disease specialist.
Patients require no specific diet.
Patients do not require activity restrictions.
Instruct high-risk individuals to avoid handling newly imported or sick birds.
Instruct patients with psittacosis to see a physician if symptoms recur (ie, relapse).
Patients with relapses may need prolonged retreatment (eg, 3-4 wk).
Severe psittacosis requires intravenous antibiotics and hospital admission.
Isolation is not indicated during hospital stay.
Patients with psittacosis may require doxycycline, usually 100 mg IV; alternatively, consider PO administration with the same dose twice a day.
Chloramphenicol is the third drug of choice but is rarely used in the United States.
Consider changing erythromycin from intravenous to oral administration (eg, 500 mg qid).
Chloramphenicol is rarely used in the United States because it may cause agranulocytosis.
Consider changing quinolones from intravenous to oral administration.
Transfer patients with psittacosis who have acute respiratory failure to an intensive care unit.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the clinical setting. Tetracycline and doxycycline are the antibiotics of choice. Treating patients for 2-3 weeks usually prevents relapse. Clinical response occurs within 24-72 hours. Use erythromycin in children younger than 9 years and in pregnant women. Chloramphenicol is a third alternative antibiotic.
Doxycycline remains the drug of choice. Macrolide and quinolone failures have been observed.
Anecdotal reports suggest that it is effective. Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected.
Concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues.
Treats mild-to-moderate microbial infections.
Plasma concentrations are very low, but tissue concentrations are much higher, giving it value in treating intracellular organisms. Has a long tissue half-life.
DOC; inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. Continue treatment for at least 2 wk to prevent relapse.
Macrolide antibiotic; second DOC. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections. In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, administer half total daily dose q12h. For more severe infections, double the dose.
Third DOC but rarely used in the US. Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.
Inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription. Anecdotal reports suggest that this drug is effective.