Updated: Jun 27, 2008
Psittacosis 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.
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.1
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 prior to the advent of antimicrobial treatment was approximately 15-20%. The mortality rate is less than 1% with appropriate antibiotic therapy.
No race predilection is observed.
No sex predilection is observed.
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.
The incubation period 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 are variable.
Disease may range from mild insidious presentations to severe pneumonia that requires mechanical ventilation.
1. Flulike syndromes without radiographic abnormalities
2. Mild-to-moderate pneumonia
3. Severe pneumonia
4. Acute respiratory failure, sepsis, and septic shock
Psittacosis is an infectious disease caused by the obligatory intracellular bacterium C psittaci.
| Brucellosis | Pneumonia, Fungal |
| Chlamydial Pneumonias | Pneumonia, Viral |
| Infective Endocarditis | Q Fever |
| Legionnaires Disease | Tuberculosis |
| Mycoplasma Infections | Tularemia |
| Pneumonia, Bacterial | Typhoid Fever |
Coxiella burnetii infection
Francisella tularensis infection
Atypical pneumonia (all causes)
Findings 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.
Patients require no specific diet.
Patients do not require activity restrictions.
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.
Day 1: 500 mg PO
Days 2-5: 250 mg PO qd
Community-acquired pneumonia: 500 mg PO/IV qd for 7-10 d
<6 months: Not established
>6 months:
Day 1: 10 mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 5 mg/kg PO qd; not to exceed 250 mg/d
May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Documented hypersensitivity; hepatic impairment; do not administer with pimozide
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Site reactions can occur with IV route; bacterial or fungal overgrowth may result from prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function or prolonged QT intervals
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.
100 mg PO bid
Severe cases: 4.4 mg/kg IV q12h
<8 years: not recommended
>8 years and <100 lb: 2 mg/kg/d in PO/IV in 1-2 divided doses on day 1; then 1-2 mg/kg/d in 1-2 divided doses; not to exceed 200 mg/d
>8 years and >100 lb: Administer as in adults
Bioavailability decreases slightly with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity is very rare with prolonged exposure to sunlight; avoid during last half of pregnancy through 8 y
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.
500 mg erythromycin stearate/base (or 800 mg ethylsuccinate) PO qid 1 h ac for 2-3 wk
Alternatively, use 333 mg q8h; increase up to 4 g/d, depending on severity of infection
30-50 mg/kg/d (15-25 mg/lb/d) PO divided q6-8h; double dose for severe infection
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
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.
500 mg IV qid for 2-3 wk
50-100 mg/kg/d IV divided q6h for 2-3 wk
Concurrently with barbiturates, chloramphenicol serum levels may decrease while barbiturate levels may increase and cause toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum chloramphenicol levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity; chloramphenicol levels may be increased or decreased
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Use only for indicated infections, or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (ie, aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately every 2 d while in therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, anemia, or findings attributable to chloramphenicol; adjust dose in liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (ie, gray syndrome)
Inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription. Anecdotal reports suggest that this drug is effective.
400 mg PO/IV qd
<18 years: Not recommended
>18 years: Administer as in adults
Antacids and electrolyte supplements reduce absorption; loop diuretics, probenecid, and cimetidine increase serum levels; NSAIDs enhance CNS stimulating effect
May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT); ferrous sulfate decreases bioavailability (administer moxifloxacin 4 h prior or 8 h following ferrous sulfate); coadministration with drugs that prolong QTc interval (quinidine, procainamide, amiodarone, sotalol, erythromycin, tricyclic antidepressants) increase risk of life-threatening arrhythmia
Documented hypersensitivity; known QT prolongation, concurrent administration of drugs that cause QT prolongation
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); superinfections may occur with prolonged or repeated antibiotic therapy; fluoroquinolones have induced seizures in CNS disorders and caused tendinitis or tendon rupture
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psittacosis, ornithosis, parrot fever, Chlamydia psittaci, C psittaci, avian-acquired psittacosis
Klaus-Dieter Lessnau, MD, FCCP, 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
Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Artificial Internal Organs, American Thoracic Society, Physicians for Social Responsibility, and Society of Critical Care Medicine
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.
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.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Richard B Brown, MD, FACP, Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine
Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and Massachusetts Medical Society
Disclosure: Nothing to disclose.
Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
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
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
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