Pneumocystis jiroveci
Introduction
Pneumocystis jirovecii, formerly known as pneumocystis carinii has been renamed to differentiate it from the Pneumocystis that causes infection in mice. The Mouse Pneumocystis is now called P carinii, while the species that cause human disease has been renamed, Pneumocystis jirovecii.
It is not the only change that happened to this pathogen. It was previously considered to be a protozoa. However, now it has been reclassified as fungus. Its wall is consist of beta-D-glucan and chitin.
It has two forms - a trophic form and a cyst form.
Risk factos
It was first described in Europe during 2nd WW causing infection in malnourished children. Then in 1960s it was associated with haematological malignancy, and in 1980s - HIV.
We can get an idea from its history about the risk factors. We can divide them into a few groups.
1. Children group - Malnutrition, primary immunodeficiency (like SCIDS)
2. Malignancy group - Solid tumour, multiple myeloma, haematological malignancy. Haematological malignancies have a higher risk than other types of malignancy.
3. Transplant group - SOT, HSCT, organ rejection. Amongst HSCT, the allogenic transplant has a higher risk esp in the first 9 months. Amongst the SOT, the risk is highest in the first 6 months post-transplant and in heart-lung transplants and lowest in renal transplants.
4. Vasculitis group - inflammatory disease - dermatomyositis etc
5. HIV
6. Immunosuppressive drugs - steroid (especially in combination like cyclophosphamide ), TNF alpha inhibitor (infliximab), fludarabine, alemtuzumab, Temozolomide etc.
Transmission
Transmission is human to human. Up to 65% healthy individuals may have asymptomatic carriage. The carriage has been associated with COPD.
Clinical presentation
Pneumocystis pneumonia (PCP) may present with dry cough, shortness of breath, fever and dyspnoea on exertion (and in some cases at rest)
Investigation
LDH
A non-specific marker. An increased LDH with a background of risk factors may suggest PCP. However, it could be elevated in other causes of lung damage like malignancy.
Beta-D-glucan
BDG can be used to diagnose PCP in the appropriate clinical setting. BDG could be elevated in other fungal infections as well. It has a good negative predictive value.
Radiology
Diffuse, bilateral, interstitial infiltrates (ground-glass pattern in CT) in the chest x-ray is the typical finding. There are many other types of findings (Lobar pneumonia, nodules, cavitation, pneumatocele, pneumothorax etc) that have been reported.
In patients on inhalation pentamidine prophylaxis, the upper lobar consolidation could be seen as pentamidine gets deposited in the lower parts of the lungs.
Microbiology
Preferred sample - bronchoalveolar lavage, induced sputum, lung biopsy
Test -
Direct fluorescent antibody staining (used to be the common test in the NHS, now being replaced by PCR)
PCR
Other stains
Trophic form - Gram-Weigert, Wright-Giemsa, or modified Pap stains
Cyst - calcofluor white, cresyl echt violet, Gomori methenamine silver, or toluidine blue
Treatment
Preferred drug
Cotrimoxazole 15 to 20 mg/kg (based on trim) in 3-4 divided doses PO or IV.
Nowadays, many papers coming up advocating lower doses, but they are not established practice yet.
Monitor potassium level.
If cotrimoxazole allergy - Consider desensitisation.
Alternative drugs
Atovaquone
Primaquine+ clindamycin (preferred in mod-severe disease)
Trimethoprim + dapsone
Inhalation pentamidine
Duration
21 days.