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.
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.
Mortality/Morbidity
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.
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.
Warn pet owners and pet-shop and poultry workers to be aware of possible respiratory symptoms and fever.
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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 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]
The following are potential laboratory findings associated with psittacosis:
White blood cell counts are normal to mildly decreased.
Liver function test values are usually mildly increased.
The erythrocyte sedimentation rate (ESR) may be elevated.
Urinalysis may show mild proteinuria (< 3500 mg/d).
Culturing of C psittaci is possible, but this practice is avoided because it can be hazardous to laboratory personnel.
Test acute-phase serum and convalescent-phase serum 2 weeks after onset to confirm a 4-fold or greater rise in the titer. Complement fixation (CF) is not a specific test and may cross-react with other chlamydial species.
Physicians use microimmunofluorescence (MIF) and polymerase chain reaction (PCR) studies to detect different chlamydial species. PCR may develop into an early and specific detection test.
Enzyme-linked immunosorbent assay (ELISA) and direct immunofluorescence (DIF) are experimental in this setting, but physicians have used them to help diagnose C psittaci infection.
Serologic tests are the mainstays of diagnosis; however, because of the delayed appearance of specific antibodies, these tests are not helpful in emergent clinical management.
Most diagnoses are established by clinical presentation and positive antibodies against C psittaci in paired sera using microimmunofluorescence (MIF) methods.[1]
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.
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]
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
Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
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
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.
Centers for Disease Control and Prevention. Notifiable Diseases and Mortality Tables. Available at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5906md.htm. Accessed: March 4, 2013.
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.
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. Available at http://www.cdc.gov/hicpac/pdf/isolation/isolation2007.pdf. Accessed: March 4, 2013.
Schlossberg D. Chlamydia psittaci (psittacosis). Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 5th ed. Philadelphia, Pa: Churchill Livingstone; 2000. 2004-6.
Stamm WE. Chlamydial infection: psittacosis. Braunwald E, et al, eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw Hill; 1998. 1055-64.
