Psittacosis and other zoonotic pneumonias

• Psittacosis (parrot fever, ornithosis) is an atypical pneumonia caused by the obligate intracellular bacterium Chlamydia psittaci, acquired by inhaling aerosols from infected birds.
• The illness usually starts 5 to 14 days after exposure with high fever, severe headache, myalgia and a non-productive cough; physical signs may be surprisingly few.
• The hallmark clue is the exposure history: birds, poultry, pigeon or market contact, often occupational. Chest imaging shows lobar or segmental consolidation, and the white cell count is usually normal or only mildly changed while C-reactive protein and ESR are high.
• Because C. psittaci is intracellular, beta-lactams do not treat it. Doxycycline is the usual first-line drug, given as 200 mg first then 100 mg every 12 hours, for about 10 to 14 days in uncomplicated severe disease and longer when ARDS or central nervous system disease is present. ^[2]
• The disease is notifiable in many countries, although it is generally not spread from person to person and routine patient isolation is not recommended.

By the end of this page you should be able to:

1. Explain how Chlamydia psittaci reaches the human lung and why the disease looks atypical.
2. Take an animal-exposure history that separates psittacosis from other causes of atypical pneumonia.
3. Recognise the clinical, laboratory and imaging pattern of psittacosis and know when to suspect it.
4. Choose and interpret the tests that confirm it, and explain why serology is often retrospective.
5. Prescribe first-line and alternative treatment with doses, routes, durations and adjustments, including in pregnancy.
6. Compare psittacosis with Q fever, tularaemia, Legionnaires disease and inhalational anthrax.
7. Outline the public health and occupational measures that follow a case.

The organism has a biphasic life cycle: small infectious elementary bodies are inhaled into the alveoli, enter respiratory epithelial cells and macrophages, and change into the larger replicative reticulate bodies that survive in a membrane-bound inclusion. Because replication happens inside cells, ordinary beta-lactam antibiotics, which act on the bacterial cell wall, are ineffective. C. psittaci is genetically diverse and grouped into genotypes linked to host species, but for clinical practice the important point is simpler: it behaves as a typical intracellular pathogen with community-acquired pneumonia as its usual presentation.^[1][4]

Human psittacosis is part of a wider spectrum. Birds may be visibly ill with ruffled feathers, nasal discharge and weight loss, or they may carry and shed the organism while looking completely normal, sometimes for long periods. Contaminated cages, feed, water, feathers and carcasses all hold infection. Household outbreaks are well described, usually from a recently purchased bird, and single cases cluster in winter and spring in temperate regions.^[1]

Psittacosis is uncommon but almost certainly underestimated, because many cases are mild and never confirmed. Case numbers rose sharply in some regions after 2020 with the spread of metagenomic next-generation sequencing, which has made the diagnosis quicker and exposed a large reservoir of unrecognised disease.^[1]

• Where and when. Cases are reported worldwide. In the largest recent synthesis from one country, reported disease clustered in cities of the south-east and was most frequent between November and April, with a peak in December to February.^[1]
• Who. Illness can occur at any age but was concentrated in adults from about 40 to 70 years in that synthesis, with several series showing a higher proportion of men.^[1]
• Exposure. Over 60 percent of documented cases had a clear history of contact with birds, and occupational groups (poultry workers, slaughterhouse and processing staff, bird and flower market workers, pet shop staff) carried the highest risk.^[1]
• Setting. Exposures split roughly between domestic bird keeping or purchase, occupational bulk handling, and market or pet shop contact, including cleaning cages or handling excreta and sick or dead birds.^[1]
• Outbreak patterns. Most human disease is sporadic, but household, occupational and common-source outbreaks all occur.^[1]
• Livestock. Sheep, goats, cattle and horses are occasionally reported as sources, mainly around parturition, although birds remain the dominant reservoir.^[3]

There is no routine post-exposure antibiotic prophylaxis recommended for contacts and, because person-to-person spread is rare, routine patient isolation is not needed. Public health interest falls on the animal source and on finding other exposed people.^[1]

The single most useful question in the history is "Any birds?" The risk is not limited to obvious pets. Parrots, parakeets, cockatiels, budgerigars and other psittacines are classic sources, but pigeons, doves, chickens, ducks, geese and turkeys all harbour the organism. Exposure may be brief and forgotten: walking past an infected aviary, sweeping a balcony where pigeons roost, or buying a bird days before it dies. Bird markets and pet shops are recurring transmission sites.^[1]

Occupation. Poultry farmers, slaughterhouse and processing workers, veterinary staff, bird dealers, market stallholders and taxidermists are the groups most often affected, along with anyone who keeps or breeds birds.^[1]

Other risk factors are less specific: older age, smoking, chronic cardiopulmonary disease and immunosuppression (including biologic therapy) are associated with more severe disease after exposure, although the organism can make a previously healthy adult critically ill.^[2]

Everything about the illness follows from three facts. The organism is intracellular, so the body cannot clear it with ordinary antibodies or with cell-wall antibiotics; it provokes a strong inflammatory response that produces high fever and an elevated CRP and ESR out of proportion to the modest chest findings; and its lipopolysaccharide and type III secretion apparatus damage the alveolar-capillary unit and adjacent organs.

After a person inhales contaminated dust or dried respiratory secretions, the elementary bodies reach the distal airspaces, are taken up by alveolar macrophages and epithelial cells, and begin to replicate in inclusions. Reticulate bodies mature and convert back to elementary bodies over the next 48 to 72 hours, with spread to regional lymph nodes and, in disseminated disease, to liver, spleen, heart, kidneys, meninges and other organs. The infected macrophages release cytokines and prostaglandins, which explains the headache, myalgia, chills and the relative absence of prominent sputum. A patchy interstitial and alveolar process follows, producing consolidation that on imaging often involves the lower lobes and basal segments and may be multifocal.^[1][4]

Because the organism does not depend on peptidoglycan for survival, Gram stain is useless and beta-lactams are inactive. Because replication depresses local cell-mediated defences, the blood picture is often a normal or mildly raised white cell count with neutrophilia and lymphopenia, rather than the marked leukocytosis of typical bacterial pneumonia, and procalcitonin may be high or normal.

Incubation is typically 5 to 14 days.^[4]

Systemic symptoms dominate early. Fever is almost always present and may be high and prolonged; chills, rigors, fatigue, headache (often severe, sometimes unilateral or periorbital) and myalgia are common. Gastrointestinal symptoms and pharyngitis occur in some patients. The severity ranges from a mild influenza-like illness to a rapidly progressive pneumonia with multi-organ involvement.^[1][3][4]

Respiratory symptoms are often modest for the degree of fever: a dry or minimally productive cough, dyspnoea and pleuritic chest pain. Relative bradycardia is not a classic feature of psittacosis (it is more typical of Legionnaires disease and Q fever).^[2]

Extrapulmonary findings are common and are the reason psittacosis is mistaken for other diseases. Hepatomegaly and splenomegaly are well described, especially in pregnancy; raised transaminases occur in many cases. Cardiac involvement (myocarditis, endocarditis, pericarditis), meningitis, encephalitis, cranial nerve and ocular findings (conjunctivitis, uveitis, ocular hypertension) and renal impairment all occur. Thrombocytopenia is frequent in severe and gestational disease, and disseminated intravascular coagulation or haemophagocytic lymphohistiocytosis can complicate the picture. A published elderly male first presented with unilateral headache and blurred vision before any chest disease was apparent.^[3][4]

A systematic review of gestational psittacosis (32 cases) reported: fever in all cases, headache in about half, cough and dyspnoea in about half, thrombocytopenia in 81 percent, raised transaminases in 84 percent, renal impairment in 56 percent, hepatosplenomegaly in some, intensive care in 66 percent, maternal mortality 13 percent and fetal or neonatal mortality 68 percent. Eighty-one percent reported animal exposure.^[3]

Examination may show fever, tachypnoea, mild chest signs over an area of consolidation, and abdominal findings of hepatosplenomegaly. Crackles or dullness may be present but are often less striking than the fever suggests. Fundoscopy and careful neurological and abdominal examination matter because of the extrapulmonary manifestations.

The first decision is whether the patient has psittacosis at all, which rests on the bird exposure, and the second is whether an alternative zoonotic or atypical organism fits better. The table compares the five diseases the question most often raises.

More generally, psittacosis belongs to the atypical pneumonia group and resembles Mycoplasma pneumoniae, Chlamydia pneumoniae (the human chlamydia, a different organism from C. psittaci), influenza, adenovirus and COVID-19. The exposure history and the discordance between high fever and relatively quiet chest examination are what should point you toward it.^[1]

Chest imaging most often shows lobar or segmental consolidation, sometimes with ground-glass opacities, frequently in the lower lobes. Rapid radiological progression, multifocal or bilateral disease and pleural effusion occur in severe cases. CT is more sensitive than radiography in early or mild disease.^[1][3]

Blood tests are non-specific but follow a pattern: normal or mildly elevated white cell count with neutrophilia and lymphopenia, markedly raised CRP and ESR, and variable procalcitonin. Thrombocytopenia, raised transaminases, bilirubin, LDH and creatinine, and impaired renal function all occur in severe or gestational disease. Anaemia is common. Blood cultures are usually negative and are sent to exclude other pathogens. Arterial gases and a full organ function screen are needed in hospital. ^[1]

Confirmatory testing rests on three approaches:

• Serology (microimmunofluorescence, MIF). The traditional method and still the most widely available. A confirmed case usually requires either a fourfold or greater rise in antibody titre between acute and convalescent serum collected 2 to 6 weeks apart, or an IgM titre of at least 1 in 16. Serology is retrospective: results rarely reach clinical decisions in time, cross-reactivity with other chlamydiae reduces specificity, and early antibiotics blunt the antibody response.^[4]
• Molecular testing. Real-time PCR targeting the ompA or 16S rRNA genes is highly sensitive and specific and avoids the biosafety problems of culture. Multiplex respiratory PCR panels sometimes include C. psittaci, but many standard commercial panels do not, so a specific request is needed.^[4]
• Metagenomic or targeted next-generation sequencing (mNGS or tNGS) of respiratory samples, including sputum, tracheal aspirate or bronchoalveolar lavage fluid. In a recent scoping review this was the most frequently reported diagnostic approach, returning results within 24 to 48 hours in one series, with sensitivity and specificity about 80 and 73 percent against conventional microbiology; PCR, serology and culture were used less often and as complementary tools.^[1]
• Culture is discouraged for routine diagnosis. C. psittaci grows in cell culture or embryonated eggs, but it is highly infectious by aerosol and requires biosafety level 3. It also cannot be seen on Gram stain. Culture remains important for genotyping and for investigating resistance and outbreaks.^[4]

Diagnostic criteria. A laboratory-supported diagnosis is made when at least one of the following holds: a fourfold rise in paired sera, a single IgM titre of at least 1 in 16, or detection of C. psittaci DNA by PCR or sequencing in a respiratory specimen. In a compatible clinical illness with a bird exposure and no other explanation, treatment is started before any result returns.^[4]

Assess severity with the same measures as for any community-acquired pneumonia: respiratory rate, oxygen saturation, blood pressure, confusion, multilobar involvement and laboratory derangement. Hospitalise patients with hypoxaemia, marked tachypnoea, hypotension, confusion or rapid radiological progression. Give oxygen, intravenous fluids, venous thromboprophylaxis and nutritional support. Critical care is needed for ARDS, septic shock or organ failure; extracorporeal membrane oxygenation has been used as rescue therapy for refractory hypoxaemia in severe psittacosis. Systemic corticosteroids are sometimes given in severe ARDS, but psittacosis-specific evidence is very limited and contemporary severe community-acquired pneumonia guidance (for example hydrocortisone when CAPE-COD criteria are met) is the pragmatic reference.^[2]

C. psittaci is intrinsically resistant to beta-lactams, so an empiric regimen that is only a beta-lactam will not treat it. Severe community-acquired pneumonia is usually covered by a beta-lactam plus either a macrolide or a respiratory fluoroquinolone, which also hits atypical organisms while the aetiology is still unknown. When there is a strong bird or market exposure and severe disease, add doxycycline or use a respiratory fluoroquinolone-containing regimen rather than waiting for confirmation.^[2]

If the diagnosis is confirmed but the patient is stable, de-escalate to a single intracellular agent.

Doxycycline is the default backbone for confirmed or strongly suspected severe psittacosis in adults.^[2][4]

• Dose: 200 mg loading dose, then 100 mg every 12 hours, intravenously or orally, according to gut function, haemodynamic stability and absorption.
• Adjustment: no routine renal adjustment, including during haemodialysis or continuous renal replacement therapy; use cautiously in severe hepatic impairment.
• Duration: about 10 to 14 days for uncomplicated severe disease, 14 to 21 days for ARDS, multilobar or extrapulmonary disease, and 21 to 28 days for confirmed central nervous system involvement.^[2]

Moxifloxacin (400 mg every 24 hours, intravenously or orally) is generally the most attractive alternative or adjunct: it is active intracellularly, is given once daily and is cleared mainly by non-renal routes. Levofloxacin is acceptable but needs renal dose adjustment in moderate or severe renal impairment, which matters in the AKI-prone intensive care population. The principal safety concern with respiratory fluoroquinolones is QT prolongation, which is greatest with co-administered macrolides, antiarrhythmic drugs, haloperidol, ondansetron or azole antifungals, or with hypokalaemia, hypomagnesaemia, structural heart disease or shock-related myocardial injury. Baseline and follow-up electrocardiography are reasonable in ventilated or vasopressor-dependent patients.^[2]

Minocycline (200 mg loading, then 100 mg every 12 hours, intravenously or orally) is preferred when central nervous system involvement is confirmed, because it penetrates the central nervous system better than doxycycline. It is not a routine substitute for doxycycline in pneumonia without central nervous system disease. ^[2]

Azithromycin (500 mg once daily for 7 to 14 days, response-guided) is the preferred targeted regimen for mild to moderate gestational psittacosis, and retains a narrow role in non-pregnant adults when both tetracyclines and fluoroquinolones are unsuitable. Intravenous azithromycin (500 mg once daily) may be used as part of empiric severe community-acquired pneumonia coverage when atypical infection is suspected.^[2]

Tigecycline (high dose) is a salvage or mixed-infection option, not routine first-line: 200 mg loading, then 100 mg intravenously every 12 hours, which is double the maintenance dose of the standard community-acquired bacterial pneumonia regimen (100 mg loading, then 50 mg every 12 hours). Reduce the maintenance dose in severe hepatic impairment; no renal adjustment is needed. Nausea, vomiting, pancreatitis, hepatotoxicity, coagulopathy and gut microbiome disturbance occur, and there is a boxed warning regarding excess all-cause mortality in non-approved indications. Apparent failure on doxycycline should prompt reassessment before any tigecycline escalation.^[2]

Omadacycline (200 mg intravenously on day 1, or 100 mg every 12 hours for two doses, then 100 mg intravenously once daily) is a renal-sparing alternative when acute kidney injury is present at presentation, continuous renal replacement therapy is anticipated, intravenous doxycycline access or oral absorption is unreliable, or in selected salvage scenarios. Oral 300 mg once daily needs strict 4-hour pre-dose and 2-hour post-dose fasting, which is impractical on continuous enteral feeding. It requires no dose adjustment in renal or mild hepatic impairment. Evidence in psittacosis is narrower than for doxycycline, and routine first-line use over doxycycline is not supported.^{[2] [4]}

Combination therapy. Routine combination of doxycycline with a fluoroquinolone or macrolide for every patient is not evidence-supported. In unstable patients with shock, substantially delayed diagnosis or unresolved coinfection concern, a temporary doxycycline plus moxifloxacin combination is reasonable. Where a single class achieves equivalent coverage, avoid overlapping macrolide and fluoroquinolone because of QT and interaction risk.^[2]

Apparent failure. True failure is defined at about 72 hours after starting an appropriate intracellular agent at adequate dose: persistent or worsening fever, oxygenation, haemodynamics or consolidation. Before escalating, exclude mimics (ventilator-associated pneumonia, coinfection, organising pneumonia, pulmonary embolism), audit drug exposure and re-image. Effective therapy usually produces measurable improvement within 48 to 72 hours. When true failure remains likely, salvage is chosen by the agent that failed and the dominant clinical problem, and high-dose tigecycline is one option.^[2]

In pregnancy psittacosis is severe: in 32 reported gestational cases, 66 percent needed intensive care, maternal mortality was 13 percent and fetal or neonatal mortality 68 percent.^[3]

• First-line targeted agent: azithromycin 500 mg once daily for 7 to 14 days, response-guided, for mild to moderate gestational psittacosis.^[2]
• Tetracyclines are conventionally avoided after the first trimester because of theoretical fetal effects, and respiratory fluoroquinolones are avoided unless maternal benefit clearly outweighs fetal concern.^[2]
• Doxycycline has, however, been endorsed by the US Centers for Disease Control and Prevention for life-threatening infections when the maternal benefit is thought to outweigh the fetal risk, and short doxycycline courses of 10 to 21 days have not been shown to cause clinically significant fetal dental or skeletal effects in available human data. A decision to use doxycycline in pregnancy therefore requires individual specialist multidisciplinary judgement, with doxycycline reserved for severe gestational disease that is deteriorating despite azithromycin.^[2]
• Severe gestational disease should be managed by infectious diseases, maternal-fetal medicine and intensive care together, because acute respiratory distress syndrome, disseminated intravascular coagulation, thrombocytopenia, hepatic and renal impairment and fetal loss can develop within hours. Intravenous azithromycin plus a safe broad-spectrum partner, and supportive care, are the mainstay; histopathology in reported cases shows active pathogen replication in the placenta causing placentitis and trophoblast necrosis, with fetal death often without direct fetal infection. Postpartum treatment shifts to doxycycline as the preferred targeted agent.^[3]

• Children: psittacosis is rare in children. Beyond standard weight-based practice, the open-access sources used here do not provide graded paediatric regimens for psittacosis, so specialist advice should guide treatment and dosing.
• Immunocompromised patients (including those on biologic therapy) are at increased risk of severe psittacosis after bird exposure, and are managed with the same targeted agents, sometimes for longer courses.^[2]
• Renal impairment: doxycycline generally needs no renal adjustment; omadacycline is an alternative when acute kidney injury or renal replacement therapy complicates care.
• Central nervous system disease: minocycline-based regimens are preferred.

• Respiratory: ARDS, respiratory failure, pneumothorax, pleural effusion, secondary bacterial pneumonia.
• Haematological: septic shock, disseminated intravascular coagulation, haemophagocytic lymphohistiocytosis, thrombocytopenia, anaemia.
• Visceral: acute kidney injury, hepatic dysfunction and transaminitis.
• Cardiovascular: myocarditis, pericarditis, endocarditis, thromboembolic events including deep vein thrombosis and pulmonary embolism.
• Neurological: meningitis, encephalitis, cranial nerve palsies.
• Ocular: conjunctivitis, uveitis, raised intraocular pressure.
• In pregnancy: spontaneous abortion, intrauterine death, stillbirth, preterm delivery and neonatal death.

With timely targeted therapy most patients recover fully. Reported severe-stratum inpatient mortality in contemporary multicentre cohorts of critically ill adults clusters around 8 to 9 percent.^[1][2] Delayed diagnosis, advanced age, comorbidity and pregnancy are associated with worse outcomes.

Major authorities that publish on psittacosis (including the US Centers for Disease Control and Prevention, StatPearls, the European Centre for Disease Prevention and Control, the British Thoracic Society and WHO, through its general zoonoses and severe acute respiratory infection guidance) agree on source control and exposure reduction, while national case definitions and notification routes differ.

• Source control in birds: quarantine new birds; test and treat infected birds under veterinary care; routinely damp-clean cages and floors rather than dry sweeping, which re-aerosolises organisms; provide adequate ventilation; remove and safely dispose of dead birds; keep apparently healthy carrier birds in mind.
• Personal protection: wear gloves and a mask when cleaning cages, handling sick or dead birds, or working in heavily contaminated environments; wash hands after contact; avoid mouth-to-beak contact with birds and avoid kissing birds.
• Occupational health: poultry farmers, slaughterhouse and processing workers, bird dealers, market stallholders and veterinary staff need education about the disease, including instruction to report compatible illness promptly.
• Notification: psittacosis is notifiable in many countries; suspected cases should be reported to local public health authorities, who will guide contact tracing and source investigation. Routes and legal requirements differ by country, so clinicians should check their own national system rather than assuming a uniform rule.^[1]
• Patient isolation and prophylaxis: human-to-human spread is rare. The US Centers for Disease Control and Prevention does not recommend routine patient isolation or antimicrobial prophylaxis for contacts on the basis of the transmission evidence available, although standard infection prevention for respiratory precautions should be applied where coinfection or diagnostic uncertainty exists.^[1]
• No human vaccine is available; prevention rests on controlling infection in birds and reducing human exposure. No Q fever vaccine is available in the United States either, a point relevant where the two zoonoses overlap in differential diagnosis.^[1]

• Pregnancy: see the dedicated subsection above; maternal and fetal risk is high and management is specialist led.
• Children and adolescents: disease is rare; use the same targeted agents with weight-based dosing under paediatric or infectious diseases advice.
• Older adults: often present later and with more extrapulmonary disease; comorbidity increases severity.
• Immunocompromised hosts: higher risk of severe disease; consider longer courses and lower threshold for inpatient care.

• The exposure history is the test. If a patient has fever, atypical pneumonia and bird, poultry, cage or market contact, treat for psittacosis rather than waiting for laboratory confirmation.
• Antibiotics: doxycycline 200 mg initially, then 100 mg twice daily, is cheap, oral and effective for most non-pregnant adults; avoid beta-lactam monotherapy in suspect cases.
• Diagnostics: if PCR or sequencing is unavailable, send paired serology; the result will be late but confirms the diagnosis and supports public health action. Chest radiography to document consolidation is valuable; CT is not essential.
• Prevention: damp cleaning instead of dry sweeping, basic cage hygiene and simple respiratory protection (damp cloth or paper mask) during high-risk tasks cost little and reduce risk.
• Referral: severe or pregnant patients, or any patient needing oxygen or with rapid radiological progression, should be referred early. Where intensive care and mechanical ventilation are unavailable, arrange transfer before deterioration.

Refer any patient with suspected psittacosis whose illness is severe, who is pregnant, who has neurological or cardiac involvement, who deteriorates at about 72 hours despite appropriate therapy, or who cannot receive oral medication. Notify public health at the same time. Early specialist input reduces the risk of ARDS, disseminated intravascular coagulation and pregnancy loss.

• Psittacosis is a Chlamydia psittaci intracellular atypical pneumonia acquired from infected birds, most often through inhaled aerosols.
• The diagnosis is usually made by exposure history; birds need not be visibly ill.
• Expect high fever, severe headache and myalgia with a surprisingly modest cough; splenomegaly, hepatitis, thrombocytopenia and renal impairment are common.
• White cell counts are normal or mildly raised, but CRP and ESR are high.
• Chest imaging shows lobar or segmental consolidation, often in the lower lobes.
• Beta-lactams are inactive; doxycycline 200 mg loading, then 100 mg twice daily, is the standard backbone.
• Durations are roughly 10 to 14 days for uncomplicated severe disease, 14 to 21 days for ARDS or extrapulmonary disease, and 21 to 28 days for central nervous system disease.
• Alternatives include moxifloxacin, minocycline (especially central nervous system), azithromycin, tigecycline (salvage) and omadacycline (renal-sparing).
• In pregnancy the maternal and fetal mortality are high; azithromycin is first line for mild to moderate disease and severe cases need multidisciplinary care.
• Confirmatory tests are PCR or sequencing, with serology as a retrospective confirmation and culture only in biosafety level 3.
• Q fever (livestock), tularaemia (rabbits, rodents, ticks), Legionnaires disease (water systems) and inhalational anthrax (spores) are the main conditions to distinguish.
• Psittacosis is notifiable in many countries; control depends on bird health and reducing aerosol exposure.

• Leptospirosis, brucellosis, plague and Q fever
• Pneumonia
• Anthrax
• Fever of unknown origin
• Infectious diseases general