A 45-Year-Old Man With Shortness of Breath, Cough, and Fever

Christine Kim, MD; Harold Moskowitz, MD

Disclosures

April 17, 2020

Discussion

The diagnosis of Pneumocystis jiroveci pneumonia (PJP) was based on the patient's history, physical examination, chest x-ray, chest CTA (although not required for diagnosis), and microscopic examination. The patient's induced sputum sample showed rare mixed flora; as a result, a bronchoalveolar lavage (BAL) specimen was obtained. Direct fluorescent antibody testing of the BAL specimen demonstrated P jiroveci. Additional testing, including acid-fast bacilli staining of the sputum; Cryptococcus neoformans antigen testing and serologic testing fortoxoplasmosis and syphilis. Sputnum cultures for cytomegalovirus, fungal pathogens, Legionella pneumophila, and Mycoplasma pneumoniae were negative thus, ruling out alternative diagnoses.

P jiroveci, previously known as P carinii, has been reclassified from a protozoan to a fungal organism and is one of the most prevalent AIDS-defining infections. Although Pneumocystis species resemble protozoa morphologically, the cell wall composition and nucleotide sequences are more characteristic of fungi.[1] The incidence of PJP is 0.5% in HIV-infected individuals with a CD4 count of 201-350 cells/µL and 8% in those with a CD4 count < 200 cells/µL.[2] The Pulmonary Complications of HIV Infection Study Group, which included more than 1100 individuals, found that 95% of patients with P jiroveci, infections had CD4 cell counts < 200 cells/µL. This study also showed that HIV transmission category, smoking history, and age did not predict the development of pneumonia.

The risk of developing PJP in black patients was one third of that seen in white patients.[3] Several risk factors for the development of PJP in patients who are not infected with HIV have been identified, including malignancy, immunosuppression, and solid-organ transplantation. Immunomodulators (most commonly, corticosteroids) and monoclonal antibody therapy are also associated with P jiroveci infection.[4]

P jiroveci cannot be sustained outside a host lung, and this limits research involving the organism. In addition, unique forms infect different animal species. P jiroveci is the official name for human Pneumocystis, and this organism cannot infect other animal species. Likewise, organisms found in other animals cannot infect humans. Although the transmission of P jiroveci is not well understood, current evidence supports human-to-human acquisition, probably via airborne particles. This route is favored over the previous suggestion that pneumonia develops from reservoirs of colonized P jiroveci acquired during childhood. Evidence supporting this includes the observation that the same strain of organism infects transplant patients in the same hospital.[1] Once inside a host lung, the haploid trophic form of P jiroveci is thought to adhere to type 1 alveolar cell membranes, then cluster to conjugate and progress as cysts. The cysts produce intracystic sporozoites, which are released and differentiate into trophozoites. One survival mechanism within the host lung may involve disabling phagocytic activity and reducing alveolar macrophage activation.[5]

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