Psittacosis, also known as parrot fever, is an infection caused by the obligatory intracellular bacterium Chlamydia psittaci.[1] 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.[2]
The primary route for infection is through the respiratory system.[1] 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 also has been implicated in transmission. Transient exposure to infected birds may cause symptomatic infection, even in visitors to pet shops.
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 probably is 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.[3] 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.[2, 4]
International
Psittacosis is found worldwide. The incidence seems to be increasing in developed countries, which is correlated to the import of exotic birds.
Mortality/Morbidity
The mortality rate of psittacosis prior to the advent of antimicrobial treatment was approximately 15-20%.[4] The mortality rate is less than 1% with appropriate antibiotic therapy.
Race
Psittacosis has no observed racial predilection.
Sex
Psittacosis has no observed sexual predilection.
Age
Psittacosis occurs in all age groups, including children. The infection is more common among individuals in the middle decades of life.
The incubation period of psittacosis is generally 5-14 days.[1, 6] 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
Pulse-temperature dissociation (less common)
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)
Splenomegaly (less common)
Diarrhea (rare)
Jaundice (rare)
Neurological
Severe headache (common)
Photophobia (common)
Agitation and lethargy
Dermatological - Includes facial rash (Horder spots)
Psittacosis is an infectious disease caused by the obligatory intracellular bacterium C psittaci.[1, 6]
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.[8]
Clinical laboratories employ a range of diagnostic methods to identify Chlamydia psittaci, such as culture, serology, and nucleic acid amplification techniques (NAAT). Although metagenomic sequencing has infrequently identified C psittaci, this approach is not commonly utilized. Specialized laboratories offer certain tests, whereas many general labs may lack testing capabilities for C psittaci or may focus solely on animal specimens.[9] Psittacosis, although uncommon, may be underdiagnosed due to its potential for mild presentations. Accurate diagnosis demands a detailed history of epidemiologic exposure, particularly in individuals with bird contact, including pet bird owners, veterinarians, and those in the poultry industry. Notably, outbreaks have been linked to individuals handling turkeys and ducks in poultry processing plants.[5, 9]
Close interaction with birds, particularly pet birds like parrots or parakeets, and employment in turkey and duck processing facilities, are key indicators of potential C psittaci infection. Diagnosis typically relies on serologic tests given the limited availability of culture. While commercial NAATs are scarce for C psittaci, the CDC and specialized labs offer PCR testing for accurate pathogen detection. The importance of early and accurate diagnosis is crucial, particularly in high-risk individuals, to ensure timely treatment and prevent potential outbreaks in occupational settings and communities.[5, 9]
Various methods are utilized to detect C psittaci, including culture, serological testing, and nucleic acid amplification techniques (NAAT). Culture, while effective, is time-consuming and performed by specialized laboratories, presenting challenges for quick treatment decisions as it involves cultivation in specific environments. Serological testing, conducted by many clinical labs, may yield cross-reactivity with other Chlamydia species and necessitates multiple patient visits for acute and convalescent paired sera collection. Complement fixation and microimmunofluorescent antibody tests are common serological methods. NAAT, characterized by high sensitivity and specificity, offer rapid results for treatment decisions but are not widely available in clinical settings, requiring specialized reagents and equipment. Real-time polymerase chain reaction (PCR) represents a notable NAAT method.[9]
Table. Potential Laboratory Findings Associated with Psittacosis[2, 6]
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:
Confirmed cases produce a positive culture result for C psittaci from respiratory secretions, a 4-fold increase in antibody titer in 2 serum samples obtained via CF or MIF 2 weeks apart, or immunoglobulin M (IgM) antibodies against C psittaci, as detected by MIF to a reciprocal titer of 16.
Possible cases show the presence of antibodies against C psittaci with titers of 1:32 by CF or MIF.
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.[1]
Treatment of C psittaci infection in humans typically involves tetracycline antibiotics as the first-line therapy. Oral administration of doxycycline or tetracycline hydrochloride often is sufficient for managing mild to moderate cases, whereas intravenous doxycycline hyclate is recommended for patients with severe illness. Clinicians should refer to current formularies for specific drug doses and treatment duration guidelines. Consulting with an infectious disease specialist can provide valuable guidance for individualized patient management.
Most cases of C psittaci infections show a positive response to antibiotics within 1 to 2 days, although relapses can occur. In situations where tetracyclines are not suitable or contraindicated, macrolide antibiotics are considered effective alternative treatment options. While the in vivo efficacy of macrolides for C psittaci is not definitively established, they may be recommended when tetracyclines cannot be used.
Considering the treatment approach for Rocky Mountain spotted fever as a model, if the potential benefits outweigh the risks and the alternative therapy is ineffective, tetracyclines like doxycycline can be considered even in pediatric cases. Prophylactic antibiotics are generally not routinely administered after suspected exposure to C psittaci; however, there may be specific circumstances where prophylaxis could be considered.[2]
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.[2, 5, 10]
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription. Anecdotal reports suggest that this drug is effective.
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.
Klaus-Dieter Lessnau, MD, FCCP, Former Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory, Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital
Disclosure: Nothing to disclose.
Coauthor(s)
Dora E Izaguirre Anariba, MD, MPH, Physician, Department of Medicine, Wyckoff Heights Medical Center
Disclosure: Nothing to disclose.
Farhad Arjomand, MD, Pulmonary Fellow, Department of Internal Medicine, Division of Pulmonary and Critical Care, Brooklyn Hospital Center, Cornell University School of Medicine
Disclosure: Nothing to disclose.
Jesus Lanza, MD, Fellow in Pulmonary and Critical Care Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Richard B Brown, MD, FACP, Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine
Disclosure: Nothing to disclose.
Chief Editor
Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London
Disclosure: Nothing to disclose.
Acknowledgements
Kenneth C Earhart, MD Deputy Head, Disease Surveillance Program, United States Naval Medical Research Unit #3
Kenneth C Earhart, MD is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.
References
CDC. Clinical Overview of Psittacosis. US Centers for Disease Control and Prevention. Available at https://www.cdc.gov/psittacosis/hcp/clinical-overview/index.html. January 31, 2024; Accessed: September 24, 2024.
Smith KA, Campbell CT, Murphy J, et al. Compendium of measures to control Chlamydophila psittaci infection among humans (psittacosis) and pet birds (avian chlamydiosis), 2010. J Exotic Pet Med. 2011 Jan. 20 (1):32-45.
CDC. Notifiable Diseases and Mortality Tables. US Centers for Disease Control and Prevention. Available at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5906md.htm. February 15, 2010; Accessed: September 24, 2024.
Hammerschlag MR. Chlamydia and Mycoplasmas. Porter RE. The Merck Manual of Diagnosis and Therapy. Rahway, NJ: Merck & Co Inc; April 2023.
Dickx V, Van Droogenbroeck C, Van Vaerenbergh B, Herman P, Braeckman L, Vanrompay D. Chlamydia psittaci, causative agent of avian chlamydiosis and human psittacosis: risk assessment and biosafety recommendations for laboratory use. Applied Biosafety. 2012. 17(2):82-8.
CDC. Laboratory Testing for Psittacosis. US Center for Disease Control and Prevention. Available at https://www.cdc.gov/psittacosis/php/laboratories/index.html. February 7, 2024; Accessed: September 24, 2024.
Siegel JD, Rhinehart E, Jackson M, Chiarello L, and the Healthcare Infection Control Practices Advisory Committee. 2007 Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Healthcare Settings. US Centers for Disease Control and Prevention. Available at http://www.cdc.gov/hicpac/pdf/isolation/isolation2007.pdf. November 27, 2023; Accessed: September 2024.
Laboratory Findings
Association with Psittacosis
White blood cell counts
Normal to mildly decreased
Liver function test values
Usually mildly increased
Erythrocyte sedimentation rate (ESR)
May be elevated
Urinalysis
May show mild proteinuria (< 3500 mg/d)
Culturing of C psittaci
Possible but avoided due to hazards to laboratory personnel
Acute-phase serum and convalescent-phase serum
Test 2 weeks after onset to confirm a 4-fold or greater rise in titer
Complement fixation (CF)
Not specific and may cross-react with other chlamydial species
Microimmunofluorescence (MIF) and polymerase chain reaction (PCR)
Used by physicians to detect different chlamydial species; PCR is specific
Enzyme-linked immunosorbent assay (ELISA) and direct immunofluorescence (DIF)
Experimental but used in diagnosis of C psittaci infection
Serologic tests
Mainstay of diagnosis; delayed appearance of specific antibodies not helpful in emergent clinical management
Diagnosis
Established by clinical presentation and positive antibodies against C psittaci using MIF methods
