An Observational Analysis of a Large Cohort of Pneumocystis jirovecii Pneumonia.

Pneumocystis jirovecii pneumonia (PCP) is an opportunistic fungal infection first widely recognized during the HIV/AIDS epidemic of the 1980s. With the advent of prophylactic strategies and widespread use of highly active antiretroviral therapy, the epidemiology of PCP has shifted. Today, the majority of PCP cases in industrialized nations occur in populations that are non-HIV immunocompromised [ 1–4 ]. As the rates of immunosuppression grow, the incidence of PCP has shown a similar trend [ 5 , 6 ].

While cellular immunodeficiency is classically associated with PCP, emerging data implicate humoral immune dysfunction [ 7 , 8 ]. Immunodeficiency may result from congenital disorders or be secondary to acquired conditions, including solid organ transplant (SOT), hematologic malignancies, solid organ cancers requiring chemotherapy, autoimmune disease necessitating immunosuppression, and hematopoietic bone marrow transplant (BMT). Glucocorticoid exposure remains a well-established risk factor [ 9 , 10 ]. Increasingly, cirrhosis has been recognized as a potential contributor to PCP risk [ 11 , 12 ].

Guidelines for prophylaxis in BMT and SOT recipients typically recommend coverage during the first 6 months posttransplant [ 13–15 ]. However, some studies suggest extended prophylaxis based on specific patient risk factors, such as prolonged lymphopenia [ 16 ]. Meanwhile, the increasing use of novel immunosuppressive agents for oncologic and autoimmune diseases has outpaced our understanding of PCP risk, as many of these therapies lack well-defined prophylaxis recommendations [ 17–19 ]. As a result, the majority of patients who develop PCP are not receiving prophylaxis, with retrospective studies reporting rates <20% [ 1 , 20–22 ].

Despite advancements in diagnostics and prophylaxis guideline development, PCP continues to impose substantial morbidity and mortality, especially among patients who are non-HIV immunocompromised. Although several risk factors have been identified, critical gaps persist in determining which patients warrant prophylaxis or empiric treatment when presenting with new-onset respiratory failure. To address these challenges, we describe the clinical presentation, risk factors, and outcomes of patients diagnosed with PCP across a large academic health system spanning multiple geographic locations. Our aim is to improve risk stratification, inform preventative strategies, and support earlier diagnosis and intervention in an era where non–HIV-associated PCP predominates.

METHODS

Patients and Data Collection

This study was approved by the institutional review board with a waiver of informed consent due to its retrospective design. Adult patients (≥18 years) were screened for inclusion if they had an ICD code for PCP or a positive polymerase chain reaction (PCR) result from sputum or bronchoalveolar lavage between 2017 and 2024. Patients met inclusion criteria if they satisfied the definitions for proven or probable PCP per the European Organization for Research and Treatment of Cancer/Mycoses Study Group Education and Research Consortium [ 23 ]. Proven PCP required microscopic identification of the organism. Probable PCP infection required that the patient was an immunocompromised host and had symptoms or imaging features consistent with PCP and either a β- D- glucan (BDG) level >80 pg/mL or a positive PCR assay result.

P jirovecii PCR testing was performed at a single central laboratory using a validated laboratory-developed real-time PCR assay targeting a single-copy gene [ 24 , 25 ]. Unlike conventional quantitative PCR methods that rely on cycle threshold cutoffs, this assay uses melt curve analysis to determine positivity. The same platform was used throughout the study period for all patients tested within our medical system.

Final classification of cases as active infection vs colonization was determined by the treating clinical team, often in consultation with infectious disease specialists, and was not reassessed by the study investigators. Patients considered colonized were typically asymptomatic, lacked immunosuppressive risk factors, or improved without treatment and were excluded from the analysis. Recurrent PCP infections were considered separate events.

Data were manually reviewed and entered into a REDCap database [ 26 ]. Variables collected included demographics, medical history, immunosuppression etiology, symptom characteristics, hospital and intensive care unit (ICU) admission data, treatment regimen, level of oxygen support, imaging findings, and clinical outcomes. Patients were categorized as follows: HIV, SOT, hematologic malignancy, solid tumors receiving chemotherapy, BMT, and autoimmune conditions requiring immunosuppression. Because many patients had multiple immunocompromising conditions, these categories were not mutually exclusive. A separate mutually exclusive “steroids only” cohort was created for patients receiving chronic high-dose corticosteroids without any of the cited conditions. Organ-specific comorbidities were not redundantly coded in transplant recipients unless the transplanted organ demonstrated dysfunction. Cross-sectional imaging data were also included. Empiric treatment was defined as the initiation of PCP-targeted antibiotics before microbiologic confirmation.

All PCP PCR tests performed within the health system during the study period were included to assess testing volume and annual positivity rates. The number of PCP diagnoses was indexed to total health system admissions (per 10 000 admissions annually).

Statistical Analysis

Categorical variables were summarized by counts and percentages. Normally distributed continuous variables were described by mean, standard deviation, and range, while skewed continuous variables were summarized by median, IQR, and range. Since reinfections were limited to 8 patients, each infection was treated as an independent event. A sensitivity analysis was then conducted on first-time infections.

Univariate and multivariable logistic regression analyses were used to identify factors associated with mortality. Given significant variation of age by cohort, multivariable regression for mortality for each cohort was individually performed to adjust for age. To isolate mortality differences among cohorts, we also adjusted for age, cohort, and chronic steroid use and performed a subgroup analysis in ICU patients, additionally adjusted for baseline Sequential Organ Failure Assessment (SOFA) score.

The annual number of cases of PCP overall and for each etiology of immunosuppression was plotted and modeled with log-linear regression with 95% CIs. Mortality rates overall and by etiology and their exact binomial 95% CIs were calculated and plotted accordingly.

RESULTS

A total of 1083 unique patients were screened by either an ICD code for PCP or a positive PCR assay result ( Supplementary Figure 1 ). Of these, 58 were deemed to represent colonization, and 332 did not meet criteria for proven or probable disease. The final study cohort consisted of 701 PCP infections in 693 patients, including 8 individuals with recurrent episodes. Demographics and comorbidities are shown in Table 1 . The most common immunosuppressive condition in this cohort was hematologic malignancies (226 patients, 32.2%), including leukemia (n = 52, 23.0%), lymphoma (n = 121, 53.5%), multiple myeloma (n = 35, 15.5%), and other hematologic malignancies (n = 18, 8.0%). Solid tumors treated with chemotherapy (n = 157, 22.4%) and autoimmune illnesses that required immunosuppression (n = 124, 17.7%) were the next most common, followed by SOT recipients (n = 90, 12.8%). Details of organ transplant distribution within the SOT subgroup are available in Supplementary Table 1 . Persons with HIV infection (n = 56, 8.0%) and those prescribed chronic steroids for various indications (n = 61, 8.7%) formed the smallest primary cohorts. The steroids-only cohort had heterogeneous indications, such as central nervous system tumors, interstitial lung disease, and alcohol-induced hepatitis. The miscellaneous cohort was also heterogeneous, although a large portion comprised patients with decompensated cirrhosis.

Table 2 presents diagnostic criteria, laboratory, and imaging features. Proven PCP was found in 71 patients (10.1%) while 630 (89.9%) were classified as probable. Among probable cases, 575 (91.3%) were PCR positive. BDG was measured in 381 of these, with 249 (65.4%) demonstrating elevated values ≥80 pg/mL. In 55 cases, BDG elevation was the sole diagnostic criteria (median BDG, 500 pg/mL; IQR, 201–500). Lymphopenia was common (n = 481, 68.6%) with a median absolute lymphocyte count of 0.59 cells/µL (IQR, 0.33–1.11).

The most frequently reported symptoms ( Table 2 ) included shortness of breath (n = 568, 81%), cough (n = 388, 55.3%), and fever (n = 265, 37.8%). Eleven patients (1.6%) were asymptomatic, and diagnosis was based exclusively on imaging abnormalities. Chest computed tomography scans were obtained in 675 cases (96.3%) with ground glass opacities present in 653 (96.7%) and consolidations in 345 (51.1%). Despite being described as a common imaging feature of PCP, “crazy paving” was infrequent, noted in only in 32 (4.7%) [ 27 ].

PCP diagnoses increased over the study period from 43 in 2017 to 140 in 2024 ( Figure 1 ) with an estimated annual growth rate of 15.8% (95% CI, 8.9%–23.2%). PCP PCR testing also increased from 1537 assays in 2017 to 3899 in 2024 with a growth rate of 13.6% (95% CI, 6.7%–20.9%). Test positivity was 4.2% (95% CI, 3.9%–4.5%) and remained stable. Indexed to total yearly admissions, PCP-related admissions per 10 000 increased at a growth rate of 0.8 per year (95% CI, .5–1.1).

The highest relative increase in PCP diagnoses was observed in BMT recipients (36%; 95% CI, 10.9%–66.8%), despite comprising only 8.1% of the cohort. Notable increases were also seen in patients with solid tumors receiving chemotherapy (21.1%; 95% CI, 7.4%–36.6%), hematologic malignancies (11.7%; 95% CI, 5.0%–18.8%), and SOT (28.4%; 95% CI, 10.3%–49.5%) as shown in Supplementary Figure 2 .

Treatment details and outcomes are summarized in Table 3 . Outpatient management was performed in 36 (5.1%) patients. These patients were normoxic, more often had an autoimmune disease as their primary risk factor, and were more frequently treated with atovaquone ( Supplementary Table 2 ). The median hospital length of stay was 10 days (IQR, 6–18). ICU admission was required for 292 (43.9%) with a median length of stay of 7 days (IQR, 3.5–14). Higher SOFA scores and chronic steroid use were associated with increased mortality in ICU patients ( Supplementary Table 3 ). The degree of hypoxemia varied across the hospitalized patient population. Of these patients, 295 (42.1%) required nasal cannula oxygen at most, 150 (22.6%) required intubation and mechanical ventilation, and 11 (1.6%) required extracorporeal membrane oxygenation for severe refractory hypoxemia.

Trimethoprim-sulfamethoxazole was the most commonly used therapy (n = 538, 76.6%), followed by atovaquone (n = 114, 16.3%). Empiric treatment prior to diagnostic confirmation was initiated in 17.7% of cases, more commonly in ICU patients (20.9%) than non-ICU patients (16.9%).

Overall mortality was 20.0% (95% CI, 17%–23%). In-hospital mortality was 21.1% with ICU mortality reaching 41.1%. Among patients who survived to discharge, 33 (6.3%) were discharged to hospice. Therefore, a composite outcome of in-hospital death or discharge to hospice was 24.7%. Mortality by cohort is shown in Supplementary Figure 3 . Patients with cirrhosis had the highest mortality rate at 50.0% (95% CI, 30.3%–68.7%), followed by patients with solid tumors receiving chemotherapy at 27.4% (95% CI, 20.6%–35.1%). Kaplan-Meier survival curves of all patients and the individual etiologies of immunosuppression are shown in Supplementary Figure 4 .

Univariate and multivariable regression analyses for mortality are shown in Table 4 . Patients with solid tumors undergoing chemotherapy had the highest odds of death (odds ratio [OR], 1.74; 95% CI, 1.15–2.63; P = .009). HIV had the lowest mortality rate at 5.4% (95% CI, 1.1%–14.9%) with an OR of death of 0.21 (95% CI, .06–.68; P = .009). Other significant univariate predictors of mortality included age (OR, 1.02 per year; 95% CI, 1.01–1.03; P = .006), cirrhosis (OR, 4.37; 95% CI, 2.08–9.17; P < .001), lower albumin (OR, 0.29; 95% CI, .20–.42; P < .001), and high lactate dehydrogenase levels (OR, 1.012 per 10 units; 95% CI, 1.01–1.02; P < .001). Chronic corticosteroid use was also associated with increased univariate mortality (OR, 1.51; 95% CI, 1.03–2.19; P = .033). In the multivariable model that adjusted for age and etiology of immunosuppression, chronic steroid use trended toward higher mortality (OR, 1.45; 95% CI, .96–2.20; P = .079). Biologic sex and body mass index were not predictive of mortality.

After adjustment for age, the OR of mortality for cirrhosis increased to 6.24 (95% CI, 2.84–13.69; P < .001). Independent of overlapping cohorts and chronic steroid use, patients with cirrhosis were estimated to have higher odds of mortality (5.60; 95% CI, 2.33–13.45; P < .001); this disparity may be attributable to higher baseline disease severity for such patients as evidenced by the nonsignificant OR in the ICU subgroup analysis adjusted for SOFA score. Mortality for patients with solid tumors receiving chemotherapy remained significantly higher after adjusting for age with an OR of 1.66 (95% CI, 1.09–2.51; P = .018), but the OR was no longer significant after adjusting for chronic steroid use. Although patients with HIV were much younger on average, their OR of death remained low at 0.27 (95% CI, .08–.90; P = .033) when adjusting for age, but similar to the solid tumor cohort, the mortality differences were no longer significant after adjusting for chronic steroid use. Sensitivity analysis limited to first-time infections did not result in any changes to the univariate and multivariable regression conclusions.

DISCUSSION

In this retrospective multicenter study, we observed a rising number of PCP diagnoses and PCP-related hospital admissions per 10 000 total admissions over an 8-year period, predominantly among patients who are non-HIV immunocompromised. However, given the retrospective design of this study, it remains unclear whether this trend represents a true increase in disease incidence or heightened clinical awareness and broader testing practices—particularly given the relatively stable PCR assay positivity rate throughout the study period. While broader adoption of PCR has contributed to increased recognition of PCP, the PCR assay used within our health system remained consistent throughout the study period. This suggests that the observed rise in cases reflects a true increase in clinical diagnoses rather than a shift in testing methodology.

The largest increases in PCP diagnoses were observed in patients with solid tumors undergoing chemotherapy, hematologic malignancies, and SOTs. These findings highlight evolving at-risk populations and underscore the need for more refined risk stratification strategies to support earlier diagnosis and prophylaxis in high-risk groups.

Despite the high burden of immunosuppression, prophylaxis rates were low at 5.4%, consistent with rates reported by other centers [ 20 , 21 , 28 , 29 ]. Existing prophylaxis guidelines primarily target early posttransplant periods and do not adequately address prophylaxis in patients receiving novel therapies or in other at-risk populations. While protocolized prophylaxis has proven highly effective in decreasing the incidence of PCP in BMT and SOT recipients, no standard guidance exists for patients receiving chemotherapy for solid tumors, despite their elevated mortality risk in this study [ 29 , 30 ]. Given the expanding list of therapies used, universal prophylaxis guidelines may not be feasible, but targeted strategies are urgently needed.

Only 17.7% of patients received empiric treatment for PCP. Notably, 50% of patients with HIV were treated empirically before microbiologic confirmation, as opposed to only 14.9% of patients without HIV. This disparity reflects the well-established PCP risk in HIV and the persistent underrecognition of risk in non-HIV populations. Improving empiric treatment rates in patients without HIV at high risk could positively influence outcomes, especially given the often rapid progression of disease.

Among patients who were HIV positive, 34% met criteria for proven PCP, as compared with only 8% of patients without HIV. This discrepancy is a well-described phenomenon attributed to the lower organism burden typically observed in non-HIV hosts [ 31 ]. For example, Bienvenu et al [ 32 ] analyzed 604 patients and found a proven diagnosis rate of only 18.9% among patients who were non-HIV immunocompromised. In our cohort, cytologic examination on bronchoalveolar lavage was performed in just 67.9% of patients without HIV. Sputum PCR was commonly used in our cohort and was positive in 154 patients who were non-HIV immunocompromised, which often obviated the need for bronchoscopy, limiting the opportunity for cytologic confirmation. Additionally, 55 patients in our cohort lacked PCR confirmation yet demonstrated markedly elevated BDG levels (median, 500 pg/mL). Taken together, these findings reinforce the diagnostic challenges of PCP in non-HIV populations and the central role of PCR in current clinical practice.

Age was a significant risk factor for mortality, consistent with findings from other studies [ 3 , 33 ]. Additionally, univariate modeling suggests a lower OR for mortality in patients with HIV and a higher OR for patients with solid organ tumors, findings corroborated in the literature [ 3 , 21 , 34 ]. Patient age differed across the various etiologies of immunosuppression; therefore, multivariable regressions adjusted for the effect of age were performed. After age adjustment, the OR for mortality remained significantly low in the HIV cohort and high in solid tumor cohort. However, after adjusting for the use of chronic steroids, the OR for mortality was no longer significant for the solid tumor cohort.

Adjunctive corticosteroids were administered to 70.9% of patients overall and in 71.2% of patients who were non-HIV immunocompromised. While corticosteroids are established in HIV-related PCP with moderate to severe hypoxemia, their role in the treatment of PCP outside of HIV remains uncertain [ 35 , 36 ]. In our cohort, corticosteroid use was largely influenced by severity of disease from 19.4% of outpatients to 73.7% in hospitalized patients and 88% in patients requiring mechanical ventilation. A separate study that further explores timing, dosing, and outcomes with corticosteroid use is currently underway.

Importantly, patients with decompensated cirrhosis are increasingly reported to be at risk for the development of PCP [ 11 , 12 ]. In our cohort, 30 patients with decompensated cirrhosis developed PCP, including 14 in whom cirrhosis was the sole identifiable risk factor. As cirrhosis is not classically recognized as a sufficient risk factor for PCP, these patients are primarily included in the miscellaneous (14/30, 46.7%) and steroids-only (10/30, 33%) classifications. This subgroup experienced the highest mortality (50.0%) with an age-adjusted OR of death of 6.24 (95% CI, 2.84–13.69; P < .001). A separate study has now been published that more comprehensively characterizes this subgroup, including clinical features, outcomes, and underlying mechanisms of immunosuppression [ 37 ].

This study has a number of limitations. Owing to its retrospective design, causality cannot be implied from the aforementioned associations. Misclassification of colonization may have contributed to the rise in diagnoses. However, this is felt to be unlikely given the unique PCP PCR and the individualized assessment of each patient to ensure that diagnostic criteria are met before entry into the study. As a tertiary referral center, our institution sees a high prevalence of patients with organ transplants, oncologic diagnoses, and complex autoimmune diseases. The relatively low proportion of patients with HIV in our cohort may reflect these referral patterns and limit the generalizability of our findings to centers with a larger HIV population. Finally, we cannot draw definitive conclusions about incidence trends due to a lack of population-level denominators and the influence of increased testing over time.

CONCLUSION

PCP is an opportunistic infection associated with significant morbidity and mortality, particularly among patients who are non-HIV immunocompromised. In one of the largest multicenter cohorts of PCP infection, we observed an increase in diagnoses that paralleled an increased testing volume. Low rates of prophylaxis and empiric treatment underscore an urgent need to better define sufficient risk and modernize preventative strategies. Patients with solid tumors receiving chemotherapy and cirrhosis are at a particularly high risk of mortality yet are not currently included in routine prophylaxis guidelines. These findings reflect a shifting landscape of PCP in the current era—driven by evolving immunosuppressive therapies and underrecognized vulnerabilities. Prospective studies and detailed analyses of these subgroups are essential to define sufficient risk and inform future prophylaxis and treatment strategies.

Supplementary Material

Contributor Information

Aaron M Pulsipher, Department of Critical Care, Mayo Clinic, Phoenix, Arizona, USA.

Holenarasipur R Vikram, Division of Infectious Diseases and Transplant Center, Mayo Clinic, Phoenix, Arizona, USA.

Michael B Gotway, Division of Cardiothoracic Radiology, Mayo Clinic, Phoenix, Arizona, USA.

Rodrigo Cartin-Ceba, Department of Critical Care, Mayo Clinic, Phoenix, Arizona, USA.

Kyle J Henry, Department of Critical Care, Mayo Clinic, Phoenix, Arizona, USA.

Alec M Johnson, Division of Infectious Diseases and Transplant Center, Mayo Clinic, Phoenix, Arizona, USA.

Ryan R Gassner, Department of Internal Medicine, Mayo Clinic, Phoenix, Arizona, USA.

Kevin Zhou, Department of Internal Medicine, Mayo Clinic, Phoenix, Arizona, USA.

Dani B Green, Department of Internal Medicine, Mayo Clinic, Phoenix, Arizona, USA.

Emily R Thompson, Division of Clinical Trials and Biostatistics, Mayo Clinic, Phoenix, Arizona, USA.

Andrew H Limper, Division of Pulmonary and Critical Care, Mayo Clinic, Rochester, Minnesota, USA.

Ayan Sen, Department of Critical Care, Mayo Clinic, Phoenix, Arizona, USA.

Augustine S Lee, Department of Allergy and Pulmonary Medicine, Mayo Clinic, Jacksonville, Florida, USA.

Kealy Ham, Department of Critical Care, Mayo Clinic, Phoenix, Arizona, USA.

Supplementary Data

Supplementary materials are available at Open Forum Infectious Diseases online . Consisting of data provided by the authors to benefit the reader, the posted materials are not copyedited and are the sole responsibility of the authors, so questions or comments should be addressed to the corresponding author.

Notes

Author contributions. Concept and design: A. M. P., K. H., H. R. V., M. B. G., A. H. L., A. S. Acquisition, analysis, or interpretation of data: all authors. Drafting of the manuscript: A. M. P., K. H., E. R. T. Critical review of the manuscript for important intellectual content: H. R. V., M. B. G., R. C.-C., K. J. H., A. M. J., R. R. G., K. Z., D. B. G., A. H. L., A. S. L., A. S. Statistical analysis: E. R. T., A. M. P., R. C.-C. Supervision: K. H., H. R. V., A. H. L., A. S., A. M. P.

Financial support. This work was supported by the Center for Clinical and Translational Science, Mayo Clinic (for REDCap support; UL1TR002377).

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Associated Data

Supplementary Materials