Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Identify Pneumocystis jirovecii pneumonia in HIV and non-HIV immune suppression, grade gas-exchange impairment, secure respiratory evidence without destabilising the patient, and deliver co-trimoxazole, selected corticosteroids and prevention safely. Confirm treatment against current BHIVA, BNF, eMC and local HIV, haematology or transplant protocols.
Pneumocystis jirovecii is an opportunistic fungus with a distinctive alveolar syndrome. In untreated HIV, PJP often evolves over days to weeks with fever, non-productive cough and progressive exertional dyspnoea at low CD4 counts. In non-HIV immune suppression it can progress faster, with a lower organism burden, more intense inflammation and abrupt respiratory failure. The different biology affects diagnostic yield and the strength of evidence for adjunctive corticosteroids.
Gas-exchange impairment may be more severe than auscultation or the first radiograph suggests. Exercise desaturation can be an early clue, while established disease causes diffuse alveolar injury and a widened alveolar-arterial oxygen gradient. CT ground-glass opacities, sometimes with cysts or pneumothorax, are supportive but overlap with viral pneumonitis, drug toxicity, oedema, diffuse alveolar haemorrhage and other fungi.
Loss of effective cellular immunity permits Pneumocystis proliferation, particularly when HIV is undiagnosed, untreated or preventive therapy is absent.
Sustained systemic corticosteroids impair T-cell and macrophage function and are a major risk outside HIV, especially with additional immune treatments.
Haematological malignancy, solid-organ or stem-cell transplantation and associated immunosuppression create high-risk host states, and several contributors may coexist in the same patient.
Biological and cytotoxic treatments for autoimmune or malignant disease can confer risk according to regimen, cumulative immune effect and local prophylaxis policy.
In impaired cellular immunity, Pneumocystis adheres to alveolar epithelium and multiplies within air spaces, which links the underlying lesion to the observed respiratory dysfunction.
Organisms, proteins and cellular debris accumulate diffusely, interfering with surfactant and ventilation, with effects that increase as the pathological process progresses.
Host immune responses thicken the alveolar-capillary interface, with the inflammatory pattern differing between HIV and non-HIV hosts.
Diffuse ventilation-perfusion mismatch and diffusion limitation cause exertional then resting hypoxaemia, often disproportionate to early auscultatory findings.
Two or more weeks of fever, dry cough, progressive exertional breathlessness, weight loss and oral candidiasis or another clue to advanced HIV. Resting observations can initially be deceptively mild.
A patient receiving corticosteroids, chemotherapy, transplant immunosuppression or a T-cell-active biologic develops rapidly increasing oxygen needs and bilateral ground glass over days.
Cyanosis, respiratory fatigue, PaO2 below 9.3 kPa or a markedly widened alveolar-arterial gradient indicates significant disease. Early critical-care involvement is appropriate if oxygen needs rise.
Pneumatoceles can complicate PJP and predispose to spontaneous pneumothorax. Sudden pleuritic pain, unilateral loss of breath sounds or acute desaturation requires immediate assessment.
COVID-19, CMV, bacterial pneumonia, TB, pulmonary oedema, drug pneumonitis, lymphoma and diffuse alveolar haemorrhage may coexist or resemble PJP; focal lobar consolidation should broaden the search.
COVID-19, cytomegalovirus and other viral infections produce similar bilateral ground-glass change; respiratory molecular testing and host context discriminate.
Focal consolidation, purulent sputum and bacterial cultures favour ordinary infection, though coinfection is possible, with targeted examination and testing used to resolve the uncertainty.
The same immune treatments that create risk can cause inflammatory toxicity; medicine timing and targeted respiratory sampling are critical.
Volume overload and cardiac dysfunction in renal or cancer care can mimic diffuse pneumonitis but have supporting haemodynamic features.
Tumour infiltration may cause diffuse interstitial change and systemic symptoms; tissue may be needed when infection tests are non-diagnostic.
Progressive diffuse gas-exchange loss may require high-level oxygen or ventilation, with potentially abrupt deterioration in non-HIV immune suppression.
Cystic or subpleural lung injury can rupture, producing recurrent or bilateral pleural air and difficult ventilatory management.
Recovering immunity after HIV treatment can transiently worsen pulmonary inflammation despite microbiological response, adding morbidity beyond the initial pulmonary disorder.
Antimicrobial therapy can cause rash, cytopenias, renal injury, electrolyte disturbance and important drug interactions, creating an additional need for recognition and targeted treatment.
Persistent immune suppression without effective prevention leaves substantial risk of another episode after apparent recovery, particularly when baseline cardiopulmonary reserve is limited.
Co-trimoxazole treatment is prescribed by milligrams of trimethoprim per kilogram per day. Confusing this with the combined tablet weight causes serious dosing error.
Lower organism burden may reduce microscopy yield, while a brisk inflammatory response causes rapid respiratory failure. A negative non-invasive sample deserves careful interpretation.
Exertional desaturation and CT ground glass may precede a visible chest-radiograph abnormality in a high-risk patient.
Cyst formation makes sudden air leak possible. Acute pleuritic deterioration demands immediate bedside examination and imaging, not attribution to expected PJP progression.
New PJP may be the first presentation of HIV or an unrecognised cumulative corticosteroid risk. Treating the pneumonia without addressing immunity invites recurrence.
Reassuring oneself with a normal early chest radiograph despite exertional desaturation and major immune risk.
Waiting for bronchoscopy before treating a severely hypoxaemic, high-probability patient.
Interpreting any positive PCR as disease without considering burden, host and CT.
Using the HIV corticosteroid threshold as an automatic mandate in non-HIV PJP.
Failing to monitor hyperkalaemia, marrow suppression and renal function on treatment-dose co-trimoxazole.
Discharging without ART coordination or a secondary prophylaxis plan when HIV is the cause.
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A person with newly diagnosed HIV has probable PJP and a room-air PaO2 of 8.6 kPa. Co-trimoxazole has just started. What is the best additional management?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Rash including severe cutaneous reactions, marrow suppression, hyperkalaemia, renal dysfunction, hepatitis and interactions such as methotrexate or warfarin. Monitor closely; do not underdose by confusing combined-tablet mass with trimethoprim mass.
Evidence is not equivalent in non-HIV disease. Hyperglycaemia, delirium, fluid effects and additional infection risk require surveillance; exclude or treat important co-infections.
Hypotension, dysglycaemia, pancreatitis, nephrotoxicity, electrolyte disturbance, cytopenia and QT prolongation. Requires intensive biochemical and ECG monitoring.
Primaquine can cause haemolysis and methaemoglobinaemia, particularly in G6PD deficiency. Clindamycin has substantial diarrhoea and C. difficile risk.
Less appropriate for severe disease; variable absorption, gastrointestinal effects, rash and interactions. Treatment failure should prompt exposure and diagnosis review.