What is Pneumocystis jirovecii pneumonia?

Pneumocystis jirovecii pneumonia, abbreviated to PJP, is an opportunistic fungal pneumonia. It develops mainly when the immune system cannot control the organism effectively, particularly when T-cell-mediated immunity is impaired.

Pneumocystis jirovecii was previously classified differently and was historically called Pneumocystis carinii in humans. The older abbreviation PCP remains common in guidelines, while PJP is increasingly used to reflect the correct name of the human organism.

The organism cannot be grown using routine microbiological culture methods. Diagnosis therefore relies on clinical assessment, imaging, detection of the organism or its DNA in respiratory samples, and supportive blood tests.

PJP is most strongly associated with advanced untreated HIV, but it also occurs after organ or stem-cell transplantation, during cancer treatment and in patients receiving corticosteroids or other immunosuppressive medicines.

PJP is a medical emergency when severe

Significant breathlessness, reduced oxygen levels or rapidly progressive symptoms in an immunocompromised patient require urgent hospital assessment. A routine outpatient appointment is not appropriate for suspected severe PJP.

Who develops PJP?

Before effective antiretroviral therapy and prophylaxis, PJP was one of the most frequent opportunistic infections in people with advanced HIV. Its incidence has fallen substantially where HIV is diagnosed early and treated effectively.

PJP remains an important cause of illness in people who are unaware that they have HIV, are not receiving ongoing treatment, have advanced immunosuppression or have not received appropriate prophylaxis.

In people without HIV, the population at risk has expanded because more patients now receive transplantation, chemotherapy, biological treatments, targeted cancer therapies and combinations of immunosuppressive drugs.

How does Pneumocystis spread?

Available evidence supports airborne acquisition and possible transmission between susceptible people. Disease may result from new acquisition or reactivation. Patients should not assume that PJP developed because of poor hygiene or a specific avoidable exposure.

Risk factors for PJP

Risk reflects the underlying disease, the degree and duration of immunosuppression, combinations of treatments, lymphocyte counts and whether preventive medication is being taken.

Advanced HIV

Risk rises markedly with a CD4 count below 200 cells/µL, particularly with a detectable viral load, oral candidiasis, weight loss or lack of effective antiretroviral treatment.

Prolonged corticosteroid treatment

Risk increases with dose, duration and additional immunosuppression. Prednisolone-equivalent doses around 20 mg daily for four weeks or longer are a commonly used clinical warning threshold, not an absolute rule.

Haematological malignancy

Acute lymphoblastic leukaemia, lymphoma and selected treatment regimens can substantially impair T-cell function.

Stem-cell transplantation

Allogeneic transplantation, graft-versus-host disease and ongoing immunosuppression are important indications for prophylaxis.

Solid-organ transplantation

Lung, heart, kidney and liver transplant recipients are at increased risk, particularly during periods of intensive immunosuppression or rejection treatment.

Cancer chemotherapy

Risk depends on the malignancy, lymphocyte depletion, corticosteroid exposure and the specific chemotherapy or targeted treatment used.

Autoimmune and inflammatory disease

Vasculitis, lupus, inflammatory myopathy and other conditions may confer risk through the disease itself and the combination of corticosteroids with immune-modifying therapies.

T-cell-depleting medicines

Agents such as alemtuzumab and selected regimens containing purine analogues or other lymphocyte-depleting treatments can produce substantial risk.

Primary immune deficiency

Congenital disorders affecting T-cell function and combined immunity can predispose children and adults to PJP.

Previous PJP

A previous episode usually creates an indication for secondary prophylaxis while significant immunosuppression continues.

Risk cannot be assessed from steroid dose alone

A lower steroid dose may still be important when combined with lymphopenia, chemotherapy, transplantation or another immunosuppressive medicine. Conversely, not every person taking corticosteroids requires prophylaxis. The complete treatment plan must be reviewed.

Symptoms and signs of PJP

Progressive breathlessness

Dry or minimally productive cough

Fever

Low oxygen saturation

Rapid breathing

Chest discomfort

Fatigue

Reduced exercise tolerance

Weight loss or reduced appetite

Physical examination may initially be less dramatic than the level of oxygen impairment. Some patients have few chest sounds despite marked hypoxaemia.

Presentation is often subacute, with symptoms progressing over several days or weeks.

Progressive exertional breathlessness
Dry cough
Fever and fatigue
Gradually increasing oxygen requirement
Potentially high organism burden in respiratory samples

Disease often progresses more rapidly and may become severe over a few days.

Acute breathlessness and fever
Rapidly worsening hypoxaemia
Greater risk of respiratory failure
Lower organism burden, making diagnosis harder
Frequent co-infection or competing diagnoses

How is PJP diagnosed?

No single result should be interpreted in isolation. Diagnosis combines immune risk, symptoms, oxygenation, imaging and microbiological evidence.

Assess severity immediately Oxygen saturation, respiratory rate, blood pressure and work of breathing help determine whether urgent hospital treatment is required.
Review immune risk HIV status, CD4 count, corticosteroid exposure, chemotherapy, transplantation and immune-modifying medicines are reviewed.
Obtain chest imaging Chest X-ray may show bilateral diffuse interstitial or ground-glass change, but early disease can produce a normal or non-specific radiograph.
Use CT when appropriate High-resolution CT is more sensitive and commonly shows bilateral ground-glass opacities. Cysts, nodules, consolidation or pneumothorax can also occur.
Measure oxygenation Arterial blood gas analysis can quantify hypoxaemia and the alveolar–arterial oxygen gradient in moderate or severe illness.
Obtain respiratory samples Induced sputum, bronchoalveolar lavage or another suitable sample may be examined by PCR, immunofluorescence or specialist stains.
Look for co-infection Bacterial, viral and other fungal infections may coexist, particularly in transplant and haematology patients.

Do not delay urgent treatment

When clinical suspicion is high and the patient is significantly unwell, treatment may need to begin before bronchoscopy or final PCR results. Starting treatment does not immediately prevent subsequent microbiological confirmation.

Imaging findings in PJP

Investigation	Possible findings	Important limitation
Chest X-ray	Bilateral diffuse or perihilar interstitial and ground-glass shadowing	May be normal in early disease and is less sensitive than CT
High-resolution CT	Bilateral ground-glass opacity, sometimes with septal thickening	Ground-glass change is not specific and has many alternative causes
Atypical CT patterns	Cysts, nodules, consolidation, upper-lobe disease or asymmetrical change	Atypical appearances increase the importance of obtaining a definitive diagnosis
Complications	Pneumothorax or pneumomediastinum, particularly with cystic lung change	Sudden deterioration or chest pain requires urgent imaging

PCR, sputum and bronchoalveolar lavage

Pneumocystis jirovecii cannot be cultured using routine laboratory techniques. Diagnosis therefore depends on direct detection or molecular testing.

Induced sputum

A non-invasive sample can provide a diagnosis, especially in HIV-associated PJP where organism burden may be higher. Sensitivity varies with technique and patient population.

Bronchoalveolar lavage

BAL usually provides a higher diagnostic yield and allows testing for alternative or simultaneous infections. The procedure must be balanced against respiratory stability.

PCR testing

PCR is highly sensitive for detecting Pneumocystis DNA. Quantitative results and clinical context help distinguish active pneumonia from low-level colonisation.

Microscopy and immunofluorescence

Special stains or fluorescent antibodies can visualise the organism. Diagnostic yield is influenced by organism burden and sample quality.

A positive PCR does not always prove pneumonia

Low levels of Pneumocystis DNA may be detected in colonised individuals who do not have active PJP. Symptoms, CT findings, immune risk, organism burden and β-D-glucan should be considered together.

The role of β-D-glucan in diagnosing PJP

Serum β-D-glucan is a fungal cell-wall marker that is commonly elevated in PJP. It is a supportive blood test rather than a test that identifies Pneumocystis specifically.

A raised result may strengthen suspicion when the patient has compatible immune risk, symptoms and CT findings. It can be particularly useful when obtaining induced sputum or BAL is difficult.

A low result can make PJP less likely, but its meaning depends on the assay, disease stage, pre-test probability and patient group. It should not be used alone to exclude a serious infection in a high-risk patient.

Requires only a blood sample
Can support an early diagnosis
Often sensitive in established PJP
Useful alongside CT and respiratory PCR
May help when bronchoscopy carries substantial risk

Not specific for Pneumocystis
May rise with Candida and other fungal infections
False-positive results can occur
Assay thresholds differ
Cannot replace an appropriate respiratory sample

β-D-glucan must be interpreted clinically

Major surgery, some blood products, haemodialysis materials, selected antibiotics, bacterial infection and other exposures may influence results. A raised value is evidence of possible fungal activity—not proof of PJP.

Treatment of Pneumocystis jirovecii pneumonia

Treatment depends on severity, HIV status, organ function, medication interactions, allergy history and whether the patient can absorb oral treatment.

Treatment	Clinical role	Important considerations
Trimethoprim–sulfamethoxazole	First-line treatment for mild, moderate and severe PJP	Dose is weight-based and adjusted for renal function; monitor potassium, renal function, blood count and rash
Clindamycin plus primaquine	Important alternative for moderate-to-severe disease when first-line treatment cannot be used	Check glucose-6-phosphate dehydrogenase status before primaquine
Intravenous pentamidine	Alternative treatment for moderate-to-severe PJP	Can cause renal, pancreatic, glucose, electrolyte and cardiac toxicity
Atovaquone	Alternative oral treatment for selected mild-to-moderate cases	Absorption depends on administration with food and it is not suitable for severe respiratory failure
Dapsone-based treatment	Alternative in selected patients under specialist guidance	Requires G6PD assessment and monitoring for haemolysis and methaemoglobinaemia

How long is treatment given?

HIV-associated PJP is normally treated for 21 days. Severe non-HIV PJP, particularly in haematology patients, is also commonly treated for approximately 21 days. Duration may be individualised according to immune status, clinical response, toxicity and specialist guidance.

Apparent deterioration can have several causes

Worsening oxygenation after treatment begins may reflect the inflammatory response to dying organisms, but clinicians must also consider incorrect diagnosis, inadequate drug exposure, treatment toxicity, fluid overload, pulmonary embolism, pneumothorax or a simultaneous infection.

When are corticosteroids used to treat PJP?

Adjunctive corticosteroids reduce the inflammatory deterioration that can follow treatment of moderate-to-severe HIV-associated PJP. They are most effective when started early.

HIV-associated PJP

Corticosteroids are recommended for moderate-to-severe disease, commonly defined by a room-air arterial oxygen pressure below 70 mmHg or an alveolar–arterial oxygen gradient of at least 35 mmHg.

Non-HIV PJP

Evidence is less certain. Corticosteroids may be considered in selected patients with severe hypoxaemia, but treatment should be individualised and balanced against further immune suppression.

Steroids should not be started without specialist assessment

Corticosteroids may worsen untreated bacterial, fungal or viral infection and can obscure diagnostic findings. Their role depends on confirmed or strongly suspected PJP, oxygen severity and the wider clinical picture.

Monitoring during treatment

Oxygen requirement

Oxygen saturation, arterial gases and work of breathing help identify improvement or impending respiratory failure.

Kidney function and electrolytes

Trimethoprim–sulfamethoxazole can affect creatinine and potassium, particularly with renal impairment or interacting medicines.

Full blood count

Cytopenias may result from PJP treatment, HIV, chemotherapy, transplantation or the underlying condition.

Liver function

Treatment-related liver abnormalities and competing causes need monitoring.

Drug reactions

Rash, fever, gastrointestinal effects and severe hypersensitivity reactions require clinical assessment.

Co-infections

Persistent fever or deterioration may require repeat CT, microbiology or bronchoscopy to identify another infection.

Preventing PJP with prophylaxis

Prophylaxis is preventive medication given during a period of clinically important immune suppression. Trimethoprim– sulfamethoxazole is usually preferred because it is effective and also protects against selected other infections.

Prophylaxis is generally indicated when the CD4 count is below the relevant threshold, particularly with ongoing HIV replication, and after a previous episode of PJP.

Effective antiretroviral therapy is essential
TMP-SMX is generally first choice
Stopping criteria depend on sustained immune recovery
Previous PJP usually requires secondary prophylaxis

Decisions depend on the underlying condition, treatment regimen, steroid exposure, lymphocyte depletion and duration of risk.

Allogeneic stem-cell transplantation
Selected haematological malignancy regimens
Prolonged corticosteroids with additional risk factors
Selected solid-organ transplant protocols
T-cell-depleting or high-risk targeted treatments

Preventive medicine	Role	Important considerations
Trimethoprim–sulfamethoxazole	Preferred first-line prophylaxis in most eligible patients	Regimen varies; monitor blood count, renal function, potassium and adverse reactions
Atovaquone	Alternative when TMP-SMX is contraindicated or not tolerated	Requires reliable oral absorption and administration with food
Dapsone	Alternative in selected patients	Check G6PD status and monitor for haemolysis or methaemoglobinaemia
Nebulised pentamidine	Alternative prophylaxis in selected circumstances	Does not provide the same systemic protection and requires an appropriate administration pathway

Prophylaxis should not be prescribed or stopped casually

The dose, frequency and duration depend on the indication, kidney function, blood counts, allergy history, interactions and expected duration of immune suppression. Decisions should be made by the team managing the underlying disease.

Recovery and prognosis

Outcome depends on how quickly treatment begins, the severity of hypoxaemia, the underlying disease, organ function, co-infections and whether intensive respiratory support is required.

Outcomes in HIV-associated PJP have improved greatly with antiretroviral treatment, prophylaxis, earlier diagnosis and effective anti-Pneumocystis therapy.

Non-HIV PJP often has a more rapid and severe course. Lower organism burden can make diagnosis harder, while coexisting malignancy, transplantation or systemic illness can reduce physiological reserve.

Follow-up after PJP

Follow-up may include assessment of oxygen requirement, repeat imaging where clinically indicated, medication-toxicity monitoring, review of immune treatment and a plan for secondary prophylaxis.

The role of specialist private respiratory assessment

Suspected acute PJP with low oxygen levels requires urgent hospital care. Private respiratory review is more appropriate for stable patients requiring specialist interpretation, follow-up or coordination with their HIV, oncology, rheumatology or transplant team.

Persistent breathlessness after treatment

Assessment may consider residual inflammation, organising pneumonia, pulmonary embolism, drug toxicity, infection or deconditioning.

Review of CT abnormalities

Specialist review can assess whether ground-glass change, cysts, nodules or other findings require follow-up.

Complex diagnostic uncertainty

PCR, β-D-glucan, imaging and immune risk sometimes provide conflicting information that requires integrated interpretation.

Prophylaxis risk assessment

Respiratory input may support the wider specialist team when evaluating recurrent infection, steroid exposure or previous PJP.

Ongoing cough or reduced fitness

Lung-function testing or exercise assessment may be considered after recovery when symptoms remain unexplained.

Recurrent respiratory infection

Investigation may consider immune deficiency, bronchiectasis, aspiration or another underlying respiratory condition.

When to seek urgent medical help

Suspected PJP can deteriorate rapidly

Seek urgent same-day assessment for new respiratory symptoms during significant immune suppression. Call 999 for:

Severe or rapidly worsening breathlessness
Blue or grey lips, collapse or confusion
A marked fall in oxygen saturation
Breathlessness at rest or inability to speak normally
Severe chest pain, fainting or sudden deterioration
Extreme weakness or inability to maintain fluids

Patients receiving chemotherapy, transplantation treatment, high-dose corticosteroids or intensive immunosuppression should promptly report new fever, cough or breathlessness to the team responsible for their care.

Conclusion

Pneumocystis jirovecii pneumonia is a serious opportunistic fungal infection that primarily affects people with impaired cell-mediated immunity.

Advanced HIV remains an important risk factor, but PJP increasingly occurs in people without HIV who receive corticosteroids, chemotherapy, transplantation treatment or immune-modifying medicines.

HIV-associated disease often develops gradually, whereas non-HIV PJP may progress rapidly to profound hypoxaemia and respiratory failure.

Diagnosis combines immune risk, CT imaging, oxygen assessment, respiratory PCR or microscopy and supportive tests such as serum β-D-glucan. Neither PCR nor β-D-glucan should be interpreted alone.

Trimethoprim–sulfamethoxazole is the preferred treatment. Adjunctive corticosteroids have an established role in moderate-to-severe HIV-associated PJP, while their use in non-HIV disease must be individualised.

Appropriate prophylaxis substantially reduces risk in selected patients. Because eligibility depends on the full immunosuppressive regimen, preventive treatment should be reviewed proactively by the clinical team rather than waiting for symptoms to develop.

Frequently asked questions

Are PJP and PCP the same condition?

Yes. PCP is the older and still widely used abbreviation. PJP reflects the current name of the human organism, Pneumocystis jirovecii.

Is PJP a fungal infection?

Yes. Pneumocystis is classified as a fungus, although it has unusual biological features and does not respond to many conventional antifungal medicines.

Can someone without HIV develop PJP?

Yes. PJP occurs after transplantation, cancer treatment, prolonged corticosteroid exposure and other forms of immunosuppression.

Is PJP contagious?

Airborne acquisition and transmission between susceptible people are biologically plausible and outbreaks have been reported. PJP does not spread in the same way as ordinary bacterial pneumonia, and routine isolation policies vary by setting.

Can a chest X-ray be normal?

Yes. Early PJP can produce a normal or non-specific chest X-ray. CT is more sensitive when clinical suspicion remains high.

Does a positive PCR confirm PJP?

Not always. PCR may detect colonisation as well as active pneumonia. Organism burden, symptoms, imaging and immune risk must be considered.

Does a raised β-D-glucan confirm PJP?

No. It supports the possibility of fungal infection but is not specific for Pneumocystis. Other fungal infections and false-positive causes must be considered.

What is the first-line treatment?

Trimethoprim–sulfamethoxazole is normally first-line treatment, with dosing adjusted for body weight, kidney function and severity.

Does every patient with PJP need corticosteroids?

No. They are recommended for moderate-to-severe HIV-associated PJP. Their benefit in non-HIV PJP is less certain and requires an individual decision.

Can PJP be prevented?

Preventive medication is highly effective in appropriately selected patients. Eligibility depends on HIV control, immune measurements, transplantation status and the complete immunosuppressive treatment regimen.

Can PJP return after treatment?

Yes. Recurrence is possible if immune suppression persists, which is why secondary prophylaxis is usually required until immune recovery or risk reduction.

References and further information

National Institutes of Health. Guidelines for the prevention and treatment of opportunistic infections in adults and adolescents with HIV: Pneumocystis pneumonia. View the current NIH guideline
Maschmeyer G, Helweg-Larsen J, Pagano L, et al. ECIL guidelines for treatment of Pneumocystis jirovecii pneumonia in non-HIV-infected haematology patients. Journal of Antimicrobial Chemotherapy. 2016;71:2405–2413. View the treatment guideline
Maertens J, Cesaro S, Maschmeyer G, et al. ECIL guidelines for preventing Pneumocystis jirovecii pneumonia in patients with haematological malignancies and stem-cell transplant recipients. Journal of Antimicrobial Chemotherapy. 2016;71:2397–2404. View the prophylaxis guideline
British HIV Association. Guidelines for the treatment of opportunistic infection in adults living with HIV. View BHIVA clinical guidance

Pneumocystis Jirovecii Pneumonia (PJP)

Early treatment can be lifesaving

PJP can occur without HIV