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Pneumocystis jirovecii

Pneumocystis jirovecii is a yeast-like ascomycetous fungus that causes Pneumocystis pneumonia (PCP), a serious and potentially life-threatening opportunistic lung infection primarily in individuals with weakened immune systems, such as those with HIV/AIDS, cancer, organ transplants, or immunosuppressive therapies.^[1]^[2] First identified in the early 20th century and reclassified from a protozoan to a fungus in 1988 based on genetic and biochemical evidence, P. jirovecii is ubiquitous worldwide, with airborne person-to-person transmission occurring through inhalation of spores.^[1]^[3] Many people are exposed to it during childhood and may harbor it asymptomatically in their lungs, but it only manifests as disease when host immunity is compromised, leading to attachment to alveolar cells, proliferation, and an inflammatory response that damages lung tissue and causes symptoms like fever, nonproductive cough, and dyspnea.^[1]^[3]^[2] Historically an AIDS-defining illness with high incidence in the pre-antiretroviral era, PCP incidence has declined significantly due to prophylaxis and improved HIV management, though it remains a major cause of morbidity in non-HIV immunocompromised patients, with thousands of cases reported annually in the United States.^[1]^[2]

Taxonomy and Nomenclature

Classification

Pneumocystis jirovecii is classified within the kingdom Eukaryota, phylum Ascomycota, subphylum Taphrinomycotina, class Pneumocystidomycetes, order Pneumocystidales, family Pneumocystidaceae, genus Pneumocystis, and species jirovecii.^[4] This placement reflects its phylogenetic position as an ascomycetous fungus adapted to mammalian hosts, confirmed through molecular analyses of ribosomal RNA and other genetic markers.^[5] The species is distinguished from other Pneumocystis members by strict host specificity and significant genetic divergence. For instance, P. carinii infects rats and P. murina infects mice, with interspecies DNA sequence differences exceeding 10-20% in key loci such as the mitochondrial large subunit rRNA and internal transcribed spacers, preventing cross-infection.^[6] These distinctions underscore the genus's pattern of co-speciation with hosts, where each species has evolved unique adaptations for a single mammalian reservoir.^[7] Taxonomic revisions post-2002 solidified P. jirovecii as the human-specific entity, renaming it from the former P. carinii f. sp. hominis based on multilocus sequence data demonstrating its separation from rodent pathogens.^[8] Subsequent multilocus sequencing of nuclear genes, including β-tubulin and superoxide dismutase, has further validated this human exclusivity, with no evidence of zoonotic transmission and divergence estimates supporting ancient host-pathogen divergence.^[9]

Etymology and Naming History

The genus Pneumocystis was established in 1912 by French pathologists Pierre Delanoë and Marie Delanoë, who described cystic bodies in the pulmonary alveoli of rats experimentally infected with Trypanosoma lewisi. The name combines the Greek pneumōn (lung) and kystis (bladder or cyst), alluding to the organism's characteristic habitat and thick-walled cyst forms. They designated the species as P. carinii to honor Italian parasitologist Antonio Carini, who had independently observed similar structures in guinea pig lungs two years earlier.^[10] ^[11] Initially, the pathogen causing interstitial plasma cell pneumonia in humans—first recognized in European malnourished infants during World War II—was regarded as identical to the rat form, P. carinii. In 1976, however, parasitologist Jacob K. Frenkel differentiated the human variant based on host specificity and morphological traits, proposing Pneumocystis jiroveci n. sp. to commemorate Czech protozoologist Otto Jirovec, who had described the human pathogen in premature infants in 1952. The formae specialis designation gained traction among researchers, while P. jiroveci remained unused at the time.^[6] ^[11] Molecular phylogenetic analyses in the 1990s revealed that Pneumocystis isolates are highly host-specific, confirming the human and rodent forms as distinct species. In 2002, James R. Stringer and colleagues formally proposed reviving Pneumocystis jiroveci for the human-specific organism, emphasizing its genetic divergence from P. carinii (now reserved for the rat pathogen). This renaming sparked debate, as it disrupted established medical terminology—such as "PCP" for Pneumocystis pneumonia—and raised questions about nomenclatural priority under shifting classifications from protozoan to fungal.^[12] With Pneumocystis reclassified as an ascomycete fungus, the International Code of Nomenclature for algae, fungi, and plants (ICN) mandated adjusting the specific epithet to jirovecii (with double "i" in the genitive case for surnames ending in consonants). This orthographic correction was validated in 2006 by Scott A. Redhead and colleagues, who lectotypified P. jirovecii based on Frenkel's 1976 description while resolving ambiguities from its initial protozoan-era publication under the International Code of Zoological Nomenclature. The updated name Pneumocystis jirovecii achieved broad acceptance by the mid-2010s, reflecting consensus on its taxonomic validity and facilitating precise scientific communication.^[11] ^[13]

Morphology and Lifecycle

Morphological Forms

Pneumocystis jirovecii exhibits two primary morphological forms: the trophic form and the cyst form. The trophic form consists of amoeboid, yeast-like cells measuring 1-5 μm in diameter, characterized by a thin, flexible cell wall approximately 20-30 nm thick and filopodial projections that facilitate adherence to host cells.^[14]^[15] These cells are haploid and represent the vegetative stage of the organism. The cyst form comprises thick-walled structures, typically 5-8 μm in diameter, serving as the reproductive stage and containing up to eight intracystic bodies, each about 1 μm in size.^[16]^[17] Cysts appear spherical when intact but often adopt helmet-shaped or cup-like morphologies due to partial collapse, and empty cysts may present as crescent-shaped remnants visible under microscopic examination.^[15]^[18] These forms are best observed using silver-based stains such as Gomori methenamine silver (GMS), which highlights the cyst walls in black, or immunofluorescence techniques that target specific surface antigens for enhanced visualization.^[16]^[19] Ultrastructurally, the cell wall of P. jirovecii differs notably from other fungi, lacking ergosterol in its membrane and instead incorporating cholesterol, which contributes to its resistance to certain antifungal agents.^[20] The cyst wall is rich in β-1,3-glucans as the predominant polysaccharide, forming a rigid β-glucan fibril layer, while both forms contain chitin, though in lesser amounts in trophic stages; these components, along with major surface glycoproteins, provide structural integrity and mediate host interactions.^[21]^[17] Trophic forms possess a simpler wall with minimal β-glucans and chitins, rendering them more fragile compared to the robust cyst structure.^[7]

Lifecycle Stages

The lifecycle of Pneumocystis jirovecii is biphasic, consisting of asexual and sexual phases that occur exclusively within the alveolar environment of mammalian lungs. The process begins with haploid trophic forms, which are the predominant vegetative stage and measure approximately 2–5 μm in size; these amoeboid-like cells proliferate asexually through binary fission, attaching to type I alveolar epithelial cells via surface proteins such as PcInt1 to facilitate nutrient uptake and expansion of the population.^[22]^[23] This asexual multiplication allows for rapid colonization and persistence in the host lung, with trophic forms comprising up to 90% of the parasite burden during infection.^[24] Transition to the sexual phase occurs through conjugation of compatible haploid trophic forms, though the precise triggers—potentially involving host immune signals or density-dependent factors—remain incompletely understood. Conjugated pairs undergo meiosis and subsequent mitosis within a developing cyst (ascus), a thick-walled structure (5–8 μm) containing up to eight intracystic bodies, which are equivalent to ascospores.^[22]^[23] These cysts represent a dormant, resistant stage adapted for survival in the lung microenvironment. Mature cysts undergo excystment, rupturing to release the eight ascospores, each of which germinates into a new haploid trophic form, thereby completing the cycle and perpetuating infection within the same or adjacent host alveoli.^[19] The entire developmental progression is confined to the mammalian respiratory tract, with no known free-living environmental phase.^[22] In vitro models of P. jirovecii cultivation, using co-cultures with differentiated airway epithelial cells, have provided insights into stage transitions influenced by environmental cues such as nutrient availability and hypoxia. Nutrient deprivation, mimicking alveolar stress, promotes sexual differentiation and cyst formation by stimulating pheromone secretion and conjugation, as observed in controlled axenic systems achieving productive growth.^[25] In 2023, researchers achieved the first long-term axenic cultivation of P. jirovecii over 70 days using optimized DMEM-based media at pH 8.0 and 37°C, resulting in a 42.6-fold increase in organism numbers (doubling time ~8.9 days) primarily of trophic forms, enabling further study of lifecycle dynamics and drug testing.^[26] Similarly, hypoxic conditions prevalent in infected lungs (partial oxygen pressure ~20–40 mmHg) enhance trophic form attachment and proliferation while potentially accelerating excystment, based on oxygen-gradient simulations in these models.^[27] These findings underscore the lung's physicochemical milieu as a key regulator of lifecycle dynamics, though in vivo validation remains limited due to cultivation challenges.

Reproduction

Pneumocystis jirovecii primarily reproduces sexually through a process known as primary homothallism, where haploid cells of the same mating type undergo mating facilitated by a unique mating-type (MAT) locus. This locus is a fusion of the plus (P) and minus (M) mating-type regions, containing all necessary genes for both mating types within a single genome, enabling self-fertilization without the need for opposite mating types. Genome sequencing of multiple P. jirovecii isolates has revealed this single, bifunctional MAT locus, supporting the homothallic mode as the dominant reproductive strategy.^[28]^[29] Evidence from comparative genomic analyses indicates functional genetic recombination during this sexual phase, despite the presence of only one mating type across isolates. Population genomics studies have detected signatures of meiotic recombination in natural P. jirovecii populations, suggesting that sexual reproduction generates genetic diversity even within the constraints of host-specific transmission. This recombination is crucial for maintaining variability, as observed in whole-genome comparisons showing low but detectable nucleotide diversity linked to sexual events.^[28]^[30]^[31] During the sexual phase, asci form within cysts, encapsulating the products of meiosis as ascospores, which contribute to genetic shuffling and diversity. This ascus-mediated process occurs in the host lung environment and is integral to completing the reproductive cycle. Although predominantly sexual, rare asexual reproduction has been observed, including budding of forms in in vitro cultures of airway cells, potentially allowing limited propagation outside the typical lifecycle.^[31]^[32]

Ecology and Transmission

Natural Habitat and Hosts

Pneumocystis jirovecii is an obligate fungal parasite that is strictly restricted to the lungs of humans, where it exhibits a strong tropism for alveolar spaces. As a host-specific pathogen within the genus Pneumocystis, it colonizes the respiratory tract of humans exclusively and is considered ubiquitous in human populations worldwide. In immunocompetent individuals, the organism typically remains asymptomatic, functioning as a commensal without eliciting disease.^[33]^[34] The natural habitat of P. jirovecii is confined to the alveolar environment of the human lung, particularly attaching to type I alveolar epithelial cells in the hypophase layer of pulmonary surfactant. It lacks a free-living stage in its lifecycle, relying entirely on host-derived nutrients due to genomic losses in essential metabolic pathways, such as amino acid synthesis, rendering it incapable of independent survival outside the mammalian lung. This dependence underscores its role as a persistent commensal in the alveoli of healthy hosts.^[33]^[35] Colonization prevalence of P. jirovecii varies geographically, with studies indicating higher detection rates in regions characterized by more humid climates compared to drier environments. For example, environmental analyses have correlated lower humidity and vapor pressure with reduced Pneumocystis detection, suggesting climatic influences on its distribution in human hosts.^[36] In terms of host range, P. jirovecii demonstrates absolute specificity to humans and does not infect other mammals, distinguishing it from zoonotic congeners like P. carinii in rats or P. murina in mice. Experimental cross-inoculation attempts have confirmed this barrier, with no successful transmission to non-human species observed. This human exclusivity is attributed to evolutionary adaptations in its genome that align closely with human host physiology.^[37]^[12]

Transmission Mechanisms

Pneumocystis jirovecii is primarily transmitted through airborne routes, with cysts (asci) and trophic forms aerosolized from the respiratory secretions of colonized or infected individuals serving as the infectious agents. These forms are released into the air during activities such as coughing or breathing, facilitating person-to-person spread, particularly in close-contact settings like households or healthcare facilities. Studies in animal models and human observations support this mechanism, indicating that healthy carriers can shed viable organisms asymptomatically, contributing to environmental contamination in shared spaces.^[38]^[39]^[40] Molecular epidemiology has provided compelling evidence for direct transmission, revealing clusters of identical P. jirovecii strains in outbreak settings. For instance, genotyping analyses in renal transplant units have identified common sources of infection among multiple patients, with restriction fragment length polymorphism (RFLP) and multilocus sequence typing confirming the spread of specific genotypes within these cohorts. Such investigations, including outbreaks affecting both renal and liver transplant recipients, underscore the role of nosocomial transmission in vulnerable populations, where prophylaxis lapses can amplify dissemination.^[41]^[42]^[43] The human-specific nature of P. jirovecii precludes an animal reservoir, with infections arising either from de novo acquisition in early life or reactivation of latent colonization in adults. Serological and genetic studies indicate that primary exposure often occurs in infancy through human-to-human contact, establishing asymptomatic colonization that may be transient or persistent in the lungs. In immunocompromised adults, disease manifestation can result from either reactivation of existing colonization or de novo acquisition, with molecular evidence indicating that new infections are common, particularly in non-HIV patients and in outbreak scenarios.^[44]^[45]^[46]^[47]^[48]

Colonization and Pathogenicity

_Pneumocystis jirovecii commonly colonizes the lungs asymptomatically in healthy immunocompetent adults, with prevalence rates estimated at 20% based on detection methods such as PCR on respiratory samples.^[49] This colonization is typically transient and controlled by the host immune system, involving alveolar macrophages and T-cell responses that limit fungal proliferation without causing disease.^[19] In individuals with intact immunity, the organism persists at low levels in the respiratory tract, potentially acquired through airborne transmission from carriers, but does not progress to symptomatic infection.^[50] Under conditions of immunosuppression, such as in HIV-infected patients with CD4+ T-cell counts below 200 cells/μL, latent colonization can reactivate, leading to uncontrolled replication and the development of pneumonia.^[48] Reactivation occurs due to diminished CD4+ T-cell mediated immunity, which normally restricts fungal growth, allowing P. jirovecii to proliferate within the alveoli.^[51] This shift from commensal to pathogen is facilitated by the fungus's ability to exploit impaired host defenses, particularly in scenarios of profound lymphopenia. The pathogenicity of P. jirovecii involves adherence to type I alveolar pneumocytes via surface glycoproteins, such as the major surface glycoprotein (Msg), which mediate tight attachment and initiate infection.^[19] Once attached, the organism disrupts pulmonary surfactant function through interactions with surfactant proteins and release of internal components post-lysis, leading to alveolar collapse and impaired gas exchange.^[52] This disruption, combined with induction of pro-inflammatory cytokines like TNF-α and IL-8 from epithelial cells and macrophages, results in excessive inflammation, foam cell formation, and progressive alveolar damage.^[51] P. jirovecii evades host immunity through antigenic variation in its Msg family, enabling switching of surface antigens to avoid recognition by antibodies and T-cells.^[53] Additionally, the formation of biofilm-like aggregates enhances persistence by protecting trophic forms from phagocytic clearance and promoting cluster growth in the alveolar space.^[54] These mechanisms contribute to disease progression, where massive proliferation fills alveoli with foamy exudate containing cysts and trophic forms, exacerbating hypoxia and respiratory failure in susceptible hosts.^[19]

Genomics

Genome Structure and Sequencing

The inability to culture Pneumocystis jirovecii in vitro has posed significant challenges to genome sequencing efforts, necessitating the use of metagenomic approaches from clinical samples such as bronchoalveolar lavage (BAL) fluid. The first de novo assembly of the P. jirovecii genome was achieved in 2012 using DNA extracted from a single BAL specimen from an immunocompromised patient, resulting in an 8.1 Mb draft genome composed of 356 contigs.^[55] This assembly predicted approximately 3,878 protein-coding genes, with a gene density of about 481 genes per Mb, and included annotation of the mitochondrial genome, which was separately characterized as a compact 27 kb linear structure encoding essential respiratory chain components.^[55]^[56] The haploid nuclear genome of P. jirovecii is estimated at 8-9 Mb and distributed across 12-16 chromosomes, based on pulsed-field gel electrophoresis and subsequent assemblies.^[38] Telomeres feature characteristic TTAGGG repeats, while subtelomeric regions are enriched with multicopy gene families, notably the major surface glycoprotein (msg) locus, which comprises over 100 variant genes involved in antigenic variation and located near chromosome ends.^[7] These structural elements contribute to genome plasticity, with the msg family occupying up to 10% of the genome.^[57] Comparative analyses with other Pneumocystis species, such as P. carinii (rat pathogen, ~8 Mb across ~13 chromosomes) and P. murina (mouse pathogen, ~8.2 Mb across ~13 chromosomes), reveal conserved compact architectures but reveal species-specific rearrangements and expansions in subtelomeric regions.^[7] Later assemblies, including a 2016 scaffold-level draft of strain RU7 (8.4 Mb, 3,675 protein-coding genes), refined contiguity using Illumina paired-end and mate-pair sequencing and confirmed ~5,000 total genes when including non-coding RNAs, highlighting the pathogen's adaptation to the mammalian lung niche.^[7]

Genetic Features and Evolution

Pneumocystis jirovecii exhibits several distinctive genetic features adapted to its obligate parasitic lifestyle within the mammalian lung. The genome shows a reduction in genes involved in de novo purine biosynthesis, with many such pathways lost, compelling the fungus to rely on host-derived purines through salvage mechanisms.^[58] This dependency reflects broader metabolic streamlining, minimizing energy expenditure on independent synthesis. Additionally, the major surface glycoprotein (Msg) superfamily is markedly expanded, comprising 64–179 unique genes that encode glycosylphosphatidylinositol (GPI)-anchored proteins crucial for adherence to host cells and evasion of immune responses.^[58] These expansions facilitate intimate host interactions, enabling antigenic variation that contributes to persistent colonization. The mating-type (MAT) locus further underscores reproductive adaptations, featuring a homothallic configuration where plus (matPi) and minus (matMc, matMi) genes are fused within a single ~10 kb region, promoting self-fertility without requiring opposite mating types.^[29] This primary homothallism supports obligate sexual reproduction in the host lung, as evidenced by concomitant expression of all three MAT genes during infection.^[29] Evolutionary analyses place the origins of P. jirovecii within the Taphrinomycotina subphylum of Ascomycota, diverging from ancestral lineages approximately 100–400 million years ago during the transition from environmental to mammalian-associated niches.^[59] The genus likely emerged around 140–165 million years ago in the Cretaceous period, coinciding with early mammalian diversification, and P. jirovecii specifically speciated about 65 million years ago alongside primate evolution.^[37]^[59] Host-switching events have punctuated this history, with phylogenetic evidence indicating shifts between mammalian lineages, such as between primates and other orders like rabbits or dogs, driven by overlapping host ranges and genetic barriers like chromosomal rearrangements.^[37] These events, rather than strict cospeciation, highlight adaptive flexibility, reinforced by ancient hybridizations observed in rodent-infecting species.^[37]^[59] Recent population genomics studies post-2020 have illuminated intraspecies variability in P. jirovecii, revealing a diverse genetic landscape even among asymptomatic carriers through targeted next-generation sequencing of multiple loci.^[60] These analyses uncovered previously unrecognized polymorphisms across global samples, suggesting ongoing gene flow and localized adaptation.^[60] Evidence of recombination hotspots emerges from patterns of linkage disequilibrium breakdown in variable regions, such as those encoding surface proteins, indicating sexual reproduction contributes to genetic diversity despite the fungus's clonal propagation in some contexts.^[60] Such findings, drawn from 2022 investigations, underscore the dynamic evolution within human populations and inform strategies for tracking transmission.^[60] Subsequent studies as of 2023–2024 have utilized long-read sequencing to better resolve the MSG gene repertoire, revealing greater complexity in antigenic variation, and applied deep mutational scanning to identify antifolate resistance mutations in dihydrofolate reductase, enhancing insights into drug adaptation.^[61]^[62]

Clinical Relevance

Disease Overview (PCP)

Pneumocystis pneumonia (PCP), also known as Pneumocystis jirovecii pneumonia (PJP), is an opportunistic fungal infection caused by the ubiquitous pathogen Pneumocystis jirovecii, primarily affecting immunocompromised individuals and characterized by diffuse alveolar damage, progressive hypoxia, and a foamy exudate filling the alveoli that impairs gas exchange.^[63]^[1] The disease manifests as a severe form of pneumonia, with the fungus proliferating within the lung alveoli, leading to an inflammatory response that desquamates type I pneumocytes and fills airspaces with proteinaceous material, resulting in ventilation-perfusion mismatches and respiratory failure if untreated.^[1] Untreated cases carry a near-fatal prognosis, with mortality rates approaching 90-100%, particularly in those with profound immunosuppression.^[64]^[65] The pathophysiology involves P. jirovecii trophozoites and cysts adhering to the alveolar epithelium, evading immune clearance in hosts with impaired T-cell function and triggering a dysregulated host response that exacerbates lung injury through cytokine release and surfactant disruption.^[1] This leads to consolidation and reduced lung compliance, culminating in hypoxemia that can progress rapidly to acute respiratory distress syndrome.^[63] Extrapulmonary dissemination is rare but can occur in severely immunocompromised patients, involving sites such as lymph nodes, spleen, or skin, often linked to delayed diagnosis or specific prophylaxis failures.^[1] Historically, PCP emerged as a prominent AIDS-defining illness during the HIV epidemic of the 1980s, accounting for up to 70-80% of opportunistic infections in untreated patients, but the advent of highly active antiretroviral therapy (HAART) and prophylaxis has dramatically reduced its incidence in HIV-infected individuals to less than 1 case per 100 person-years in regions with access to care.^[63] Post-HAART, the disease has shifted to broader at-risk populations beyond HIV, including transplant recipients and those on immunosuppressive therapies, underscoring its role as a marker of profound immunodeficiency across various clinical contexts.^[1]

Epidemiology and Risk Factors

Pneumocystis jirovecii pneumonia (PCP) has an estimated global incidence of over 400,000 cases annually, primarily affecting immunocompromised individuals worldwide.^[66] While the incidence of PCP among people with HIV has declined substantially due to widespread use of antiretroviral therapy (ART) and primary prophylaxis, the overall burden remains significant, with up to 60% of cases now occurring in non-HIV patients.^[63]^[67] This shift is attributed to increasing numbers of non-HIV immunocompromised populations, including those undergoing solid organ or hematopoietic stem cell transplantation and patients receiving chemotherapy for malignancies.^[68] Key risk factors for PCP include profound immunosuppression, particularly in individuals with HIV and CD4+ T-cell counts below 200 cells/μL, where the risk escalates dramatically without prophylaxis.^[69] In non-HIV patients, high-dose corticosteroids (e.g., prednisone ≥20 mg/day for ≥1 month) represent the most common predisposing factor, often in combination with other immunosuppressants, while chemotherapy-induced neutropenia in cancer patients, especially those with hematologic malignancies, also heightens susceptibility.^[70] Additionally, neonates, particularly preterm infants, exhibit higher rates of P. jirovecii colonization, which may contribute to early respiratory complications, and elderly individuals show increased colonization prevalence linked to age-related immune decline.^[71]^[72] Geographically, PCP incidence is higher in developed countries with advanced transplant programs and widespread use of immunosuppressive therapies, where non-HIV cases predominate in industrialized settings.^[73] In contrast, HIV-related PCP remains more prevalent in resource-limited regions with lower ART coverage. Outbreaks have been documented in healthcare settings, such as a 2021 cluster among kidney transplant recipients at a single U.S. hospital, highlighting potential nosocomial transmission risks in vulnerable patient groups.^[74]

Diagnosis

Diagnosis of Pneumocystis jirovecii pneumonia (PCP) relies on detecting the organism in respiratory specimens, often combined with clinical and radiographic findings, as the fungus cannot be cultured in standard media.^[75] Traditional diagnostic methods involve microscopic examination of induced sputum or bronchoalveolar lavage (BAL) fluid. Induced sputum, obtained noninvasively, or BAL, which requires bronchoscopy, are stained using techniques such as Giemsa for trophozoites and cysts or methenamine silver (GMS) for cyst walls, achieving sensitivities of 50-90% depending on the method and operator expertise; for example, GMS staining yields approximately 79% sensitivity and 99% specificity.^[75]^[20] Immunofluorescence assays, using monoclonal antibodies against surface antigens, enhance specificity (81-100%) and are particularly useful for confirming P. jirovecii in low-burden infections, though sensitivity varies from 48-100%.^[75]^[76] Molecular techniques have become the gold standard for higher sensitivity, particularly in non-HIV immunocompromised patients where fungal burden may be low. Quantitative real-time PCR (qPCR) targeting the mitochondrial large subunit ribosomal RNA (mtLSU rRNA) gene on respiratory samples like BAL or induced sputum detects P. jirovecii DNA with sensitivity exceeding 95% and specificity near 98%, often using cycle threshold (Ct) values to differentiate active infection (Ct <36) from colonization.^[75]^[76] As an adjunct, the serum (1,3)-β-D-glucan assay, a non-culture-based fungal marker, supports diagnosis with sensitivity of 90-95% and specificity of 70-90% at cutoffs ≥80-200 pg/mL, though false positives can occur with other fungal infections or procedures like hemodialysis.^[20]^[75] Post-2020 advances include multiplex PCR panels and metagenomic next-generation sequencing (mNGS), which enable rapid detection alongside other pathogens and strain genotyping for outbreak investigation. Multiplex targeted NGS on BAL fluid achieves 100% sensitivity for PCP in some cohorts, outperforming traditional PCR, while mNGS identifies P. jirovecii sequence reads for genotyping multilocus sequence types (MLST), facilitating epidemiological tracking of transmission in healthcare settings.^[77]^[78]^[60]

Treatment and Prevention

The primary treatment for Pneumocystis jirovecii pneumonia (PCP) is trimethoprim-sulfamethoxazole (TMP-SMX), administered intravenously at a dose of 15–20 mg/kg/day of the trimethoprim component (with sulfamethoxazole 75–100 mg/kg/day) divided every 6–8 hours for a duration of 21 days in moderate-to-severe cases.^[63] For patients with hypoxia (PaO2 <70 mmHg or alveolar-arterial oxygen gradient ≥35 mmHg), adjunctive corticosteroids, such as prednisone 40 mg orally twice daily for days 1–5 followed by a taper, are recommended to reduce mortality, ideally initiated within 72 hours of starting antimicrobial therapy.^[63] In mild-to-moderate PCP, oral TMP-SMX at the same dosing can be used, with a switch from intravenous to oral formulation possible upon clinical improvement.^[63] For patients intolerant to sulfa drugs, alternative therapies include intravenous pentamidine at 4 mg/kg/day for moderate-to-severe PCP or oral atovaquone at 750 mg twice daily with food for mild-to-moderate cases.^[63] Other options, such as primaquine (30 mg base orally daily) combined with clindamycin (600 mg intravenously every 6 hours or 450 mg orally every 6–8 hours), are effective alternatives, though glucose-6-phosphate dehydrogenase testing is required prior to use to avoid hemolysis.^[63] In salvage therapy for refractory PCP, echinocandins like caspofungin have shown promise in small studies, often used in combination with TMP-SMX in non-HIV immunocompromised patients.^[20] Emerging genetic studies as of 2025 suggest potential antifolate resistance in P. jirovecii, particularly in settings with prolonged prophylaxis, highlighting the need for ongoing surveillance of treatment efficacy.^[79] Prevention of PCP relies on prophylaxis in high-risk groups, with TMP-SMX as the first-line agent at a dose of one double-strength tablet (160/800 mg) orally daily or three times weekly.^[63] In patients with HIV, primary prophylaxis is indicated when CD4 counts fall below 200 cells/mm³, while secondary prophylaxis is recommended following a prior PCP episode until CD4 recovery to ≥200 cells/mm³ for at least 3 months on antiretroviral therapy.^[63] For non-HIV immunocompromised patients, such as solid organ or hematopoietic stem cell transplant recipients, TMP-SMX prophylaxis is advised during periods of intense immunosuppression, typically for 6–12 months post-transplant or longer in high-risk cases.^[20] Recent guidelines emphasize monitoring adherence to prophylaxis regimens to optimize efficacy and reduce breakthrough infections in these populations.^[20] Alternatives for intolerant patients include dapsone (100 mg orally daily, with G6PD screening) or atovaquone (1,500 mg orally daily).^[63]

History

Discovery and Early Observations

The genus Pneumocystis was first observed in 1909 by Carlos Chagas in the lungs of guinea pigs experimentally infected with Trypanosoma cruzi in Brazil, where Chagas initially mistook the cysts for a developmental stage of the trypanosome.^[80] Chagas described these structures as causing a peculiar pneumonia, noting their presence in the pulmonary alveoli of affected animals, including guinea pigs and small primates.^[38] This initial identification highlighted the pathogen's association with respiratory disease in mammals, though its distinct nature was not yet recognized.^[81] In 1912, French pathologists Pierre Delanoë and Marc Delanoë independently identified similar organisms in the lungs of wild rats in Paris, distinguishing them from other protozoa and formally naming the genus Pneumocystis carinii in honor of Italian researcher Antonio Carini, who had reported cyst-like forms in 1910.^[82] Their description emphasized the organism's cyst morphology and pulmonary tropism in rats, establishing it as a novel protozoan entity rather than a trypanosome stage.^[81] Over the following years, P. carinii was documented in various laboratory animals, including rats, mice, and rabbits, often in association with subclinical or epidemic pneumonias in overcrowded or stressed populations.^[38] Early human infections were reported in the 1930s and 1940s among malnourished infants in European orphanages, manifesting as severe interstitial pneumonia characterized by plasma cell infiltrates, now recognized as Pneumocystis pneumonia (PCP).^[83] The organism was first observed in human lung tissue in 1942 by Dutch pathologists C. van der Meer and S. L. Brug.^[84] These cases, termed "plasma cell pneumonia," occurred in epidemics, particularly in post-World War I and II settings with high rates of infant malnutrition and institutional crowding.^[85] In 1952, Czech parasitologist Otto Jirovec confirmed Pneumocystis as the causative agent of this infantile pneumonia through detailed microscopic studies, distinguishing the human pathogen from animal strains.^[86] By the 1950s, the pathogen was increasingly identified in premature and debilitated infants, with autopsy studies confirming Pneumocystis as the causative agent through microscopic detection of cysts in lung tissue.^[87] The recognition of Pneumocystis as a significant opportunistic pathogen surged in 1981 amid the emerging AIDS epidemic, when clusters of PCP cases were reported in previously healthy young men, particularly among gay men in Los Angeles and other U.S. cities.^[88] A pivotal CDC report in June 1981 detailed five cases of biopsy-proven PCP in immunocompetent-appearing individuals, linking the infections to underlying cellular immunodeficiency and marking the pathogen's role in the newly identified syndrome.^[88] This outbreak underscored Pneumocystis's dependence on host immunosuppression for clinical manifestation, transforming it from a rare pediatric entity to a hallmark of acquired immune deficiency.^[89]

Key Milestones in Research

In the 1970s, pioneering studies using isoenzyme electrophoresis demonstrated clear biochemical differences between Pneumocystis isolates from humans and rats, providing early genetic evidence for their separation as host-specific strains and challenging the notion of a single species.^[90] This work, building on antigenic and morphological observations, laid the foundation for recognizing distinct Pneumocystis variants adapted to specific mammalian hosts.^[90] During the 1980s, the development of reliable animal models, primarily in immunosuppressed rats and mice, marked a significant advance in experimental research on Pneumocystis pneumonia.^[91] These models enabled systematic investigations into transmission, pathogenesis, and therapeutic interventions, accelerating progress amid the rising incidence of cases during the AIDS epidemic.^[92] A pivotal taxonomic shift occurred in 2002 with the formal renaming of the human pathogen from Pneumocystis carinii f. sp. hominis to Pneumocystis jirovecii, honoring Otto Jirovec and reflecting accumulating genetic data on its strict human host specificity.^[6] Multilocus sequence analyses at the time confirmed minimal cross-infection potential between human and rodent strains, solidifying P. jirovecii as a distinct species.^[6] The first draft genome assembly of P. jirovecii was achieved in 2012 through high-throughput sequencing of clinical isolates, revealing a compact fungal genome of approximately 9 Mb with reduced metabolic capabilities adapted to obligate parasitism.^[55] This milestone enabled comparative genomics and identification of potential drug targets, though challenges in culturing limited initial functional annotations.^[55] Post-2020 research has advanced P. jirovecii cultivation techniques, with a 2023 report describing optimized axenic long-term culture conditions that sustained growth for over 70 days without feeder cells, overcoming a longstanding barrier to in vitro studies.^[93] Concurrently, CRISPR/Cas9 methodologies have been adapted for genetic editing in related Pneumocystis species like P. murina, facilitating functional validation of genes involved in host attachment and immune evasion, with implications for P. jirovecii pathogenesis.^[94] Vaccine development has also progressed, highlighted by post-2020 demonstrations that immunization with the KEX1 protease antigen elicits protective humoral and cellular responses in primate models, reducing Pneumocystis pneumonia severity by up to 80% in immunocompromised hosts.^[95]

References

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Jun 24, 2024 · Pneumocystis jirovecii is a fungus that is common throughout the world. Many people have been exposed to it as children. Some people have the ...
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Currently, Pneumocystis spp. has the following taxonomic status: Dominio: Eukaria; Kingdom: Fungi; Phylum: Ascomycota; Class: Pneumocystidomycetes; Subclass: ...
[6]
A New Name for Pneumocystis from Humans and New Perspectives ...
Pneumocystis organisms from different host species have very different DNA sequences, indicating multiple species. In recognition of its genetic and functional ...Missing: distinction murina
[7]
Genome analysis of three Pneumocystis species reveals adaptation ...
Feb 22, 2016 · The genomes of P. murina and P. carinii are very similar in total length, chromosome structure and gene organization, and show limited ...
[8]
A new name (Pneumocystis jiroveci) for Pneumocystis from humans
In recognition of its genetic and functional distinctness, the organism that causes human PCP is now named Pneumocystis jiroveci Frenkel 1999.
[9]
Multilocus Sequence Typing of Pneumocystis jirovecii from Clinical ...
The aim of this study was to evaluate the discriminatory power of eight distinct loci previously used for the molecular typing of P. jirovecii.Missing: taxonomic 2002
[10]
Etymologia: Pneumocystis jirovecii - PMC - NIH
He proposed the name P. jirovecii in honor of Czech parasitologist Otto Jírovec, who reported Pneumocystis as a cause of interstitial pneumonia in infants, ...
[11]
Pneumocystis and Trypanosoma cruzi: nomenclature and typifications
Pneumocystis jirovecii is lectotypified and epitypified. The rat parasite, Pneumocystis carinii, is neotypified, separating it from Pneumocystis wakefieldiae.Missing: ICN | Show results with:ICN
[12]
A New Name for Pneumocystis from Humans and New Perspectives ...
Sep 9, 2002 · Pneumocystis organisms were first reported by Chagas in 1909 (10), but he mistook them for a morphologic form of Trypanosoma cruzi. Within a ...
[13]
Spelling Pneumocystis jirovecii - PMC - NIH
The correct and valid name under ICBN is Pneumocystis jirovecii. Redhead et al. further explain the basis for this correction (5).Missing: 2015 | Show results with:2015
[14]
A Molecular Window into the Biology and Epidemiology of ...
Jun 13, 2018 · Added value of next-generation sequencing for multilocus sequence typing analysis of a Pneumocystis jirovecii pneumonia outbreak. Emerg ...
[15]
Pneumocystis - Pathology Outlines
Apr 17, 2025 · Pneumocystis jirovecii are round to oval and cup shaped GMS positive cysts, approximately the size of red blood cells, with a central dot.
[16]
DPDx - Pneumocystis - CDC
Pneumocystis jirovecii (previously classified as Pneumocystis carinii) was previously classified as a protozoa. Currently, it is considered a fungus based ...Missing: taxonomic Ascomycota
[17]
Pathobiology of Pneumocystis pneumonia: life cycle, cell wall and ...
The original name P. carinii was retained for a Pneumocystis species that co-exists with rats. Although it is likely that each Pneumocystis strain associated ...Life Cycle · Cell Wall · Clinical Disease<|control11|><|separator|>
[18]
BIOL 230 Lecture Guide - Cysts of Pneumocystis carinii
Cysts of Pneumocystis jiroveci in lung tissue, Gomori methenamine silver stain method. The walls of the cysts are stained black and often appear crescent shaped ...
[19]
Pneumocystis - PMC - PubMed Central - NIH
The genus Pneumocystis represents related fungal species that are members of the phylum/division Ascomycota, the subphylum Taphrinomycotina, class ...Missing: taxonomic | Show results with:taxonomic
[20]
Pneumocystis jiroveci Pneumonia: A Review of Management ... - NIH
Mar 24, 2023 · It lacks chitin in its cell wall and its cell membrane contains cholesterol instead of ergosterol, making it resistant to antifungal drugs ...
[21]
Targeting β-glucans, vital components of the Pneumocystis cell wall
β-glucan is the most abundant polysaccharide in the cell wall of Pneumocystis jirovecii, which has attracted extensive attention because of its unique ...Missing: ergosterol | Show results with:ergosterol
[22]
https://doi.org/10.1038/nrmicro1621
[23]
https://doi.org/10.1146/annurev.micro.112408.134335
[24]
Pneumocystis jirovecii—from a commensal to pathogen - NIH
Aug 19, 2015 · The name was given in honor of the Czech parasitologist Otto Jirovec, due to his important contribution in describing this organism in humans ( ...
[25]
https://doi.org/10.1371/journal.pone.0079958
[26]
The Persistent Challenge of Pneumocystis Growth Outside the ... - NIH
May 20, 2021 · Abstract. The pathogenic fungi in the genus, Pneumocystis, have eluded attempts to continuously grow them in an ex vivo cultivation system.Missing: influences | Show results with:influences
[27]
Comparative Genomics Suggests Primary Homothallism of ...
Jan 13, 2015 · Sexual reproduction probably occurs, but the system of this process and the mating type (MAT) genes involved are not characterized. In the ...
[28]
Functional and Expression Analyses of the Pneumocystis MAT ...
It is thought to include both asexual and sexual phases. Comparative genomic analysis suggested that their mode of sexual reproduction is primary homothallism ...
[29]
Comparative Population Genomics Analysis of the Mammalian ...
May 8, 2018 · To investigate the diversity and demographic history of natural populations of Pneumocystis infecting humans, rats, and mice, we performed whole-genome and ...
[30]
Pneumocystis Mating-Type Locus and Sexual Cycle during Infection
Jun 16, 2021 · These observations suggest that the sexual mode of reproduction of Pneumocystis species is primary homothallism, the mode that involves a single ...
[31]
Pneumocystis jirovecii Can Be Productively Cultured in ... - NIH
May 13, 2014 · This is the first report of the successful productive cultivation and propagation of Pneumocystis jirovecii, a human-pathogenic fungus of major ...
[32]
The Persistent Challenge of Pneumocystis Growth Outside the ...
May 19, 2021 · The pathogenic fungi in the genus, Pneumocystis, have eluded attempts to continuously grow them in an ex vivo cultivation system.
[33]
https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2021.681474/full
[34]
Comparative Genomics Suggests that the Fungal Pathogen ...
Comparative Genomics Suggests that the Fungal Pathogen Pneumocystis Is an Obligate Parasite Scavenging Amino Acids from Its Host's Lungs | PLOS One.Missing: habitat | Show results with:habitat
[35]
The Relationship between Pneumocystis Infection in Animal and ...
Oct 26, 2018 · Lower detection of Pneumocystis observed in 1981 corresponded with low temperature, low vapor pressure, and low humidity.
[36]
Genomic insights into the host specific adaptation of the ... - Nature
Mar 8, 2021 · To explore the evolutionary history of the Pneumocystis genus, and investigate P. jirovecii genetic factors that support its adaptation to ...Missing: distinction | Show results with:distinction
[37]
Transmission and Colonization of Pneumocystis jirovecii - PMC - NIH
Nov 18, 2021 · According to available information, it is accepted that a lifecycle of Pneumocystis spp. is comprised of two main stages: a mononuclear cell ...
[38]
Pneumocystis jirovecii detection in asymptomatic patients - NIH
May 23, 2017 · Pneumocystis thrives at the surface of type I pneumocytes in the alveolar space and is found as two main life cycle stages: the trophic form and ...<|control11|><|separator|>
[39]
Pneumocystis jirovecii: Trends in Microbiology - Cell Press
Apr 21, 2020 · Pneumocystis jirovecii is an ascomycete, specific for humans, characterized by a strong tropism for the lungs and airborne host-to-host transmission.<|control11|><|separator|>
[40]
Outbreak of Pneumocystis Pneumonia in Renal and Liver ... - NIH
This is the first reported outbreak of PCP occurring in both renal and liver transplant recipients. The outbreak was caused by three strains of Pneumocystis, as ...
[41]
Epidemiological Outbreaks of Pneumocystis jirovecii Pneumonia ...
Epidemiological Outbreaks of Pneumocystis jirovecii Pneumonia Are Not Limited to Kidney Transplant Recipients: Genotyping Confirms Common Source of Transmission ...
[42]
Investigation of outbreaks of Pneumocystis jirovecii pneumonia in ...
Nov 18, 2016 · This article describes two outbreaks of P. jirovecii pneumonia (PCP) in renal transplant patients in the West of Scotland.
[43]
Evolving spectrum of Pneumocystis host specificity, genetic diversity ...
We present this review to summarize pivotal advancements in Pneumocystis epidemiology, host specificity, genetic diversity and evolution.
[44]
New advances in understanding the host immune response to ... - NIH
It is important to note that Pneumocystis is host specific with Pneumocystis jirovecii found in humans, Pneumocystis carinii in rats and Pneumocystis murina in ...
[45]
Pneumocystis jirovecii infection: an emerging threat to patients ... - NIH
Reactivation from lifelong latency or de novo infection? It has long been debated whether PCP development is due to a reactivation of latent childhood infection ...
[46]
Colonization by Pneumocystis jirovecii and Its Role in Disease - PMC
Although reactivation of latent infection may be one mechanism of PCP infection, human and animal studies imply that de novo infection also occurs. For ...
[47]
Pneumocystis jirovecii Colonization in Non-HIV-Infected Patients ...
Studies of Nevez et al. (25) and Medrano et al. (9) using nested-PCR method have revealed a colonization rate about 20% in healthy immunocompetent adults. Also ...
[48]
Current Epidemiology of Pneumocystis Pneumonia - CDC
Most healthy persons do not have detectable Pneumocystis in respiratory specimens, but rates of colonization may be as high as 69% in HIV-infected persons (14) ...
[49]
Pneumocystis Pneumonia in Human Immunodeficiency Virus ...
PCP usually develops in HIV-infected patients when the CD4+ lymphocyte count decreases to fewer than 200 cells/mm3 and particularly to fewer than 100 cells/mm3.
[50]
Current understanding of Pneumocystis immunology - PMC
This article focuses on research conducted during the previous 5 years regarding the host immune response to Pneumocystis, including innate, cell-mediated and ...
[51]
Pneumocystis jirovecii pneumonia: a proposed novel model of ...
Jul 20, 2021 · Component 5: Post-lytic Pneumocystis jirovecii internal components bind and disrupt surfactant function. Surfactant disruption is at the ...
[52]
Variation in the Major Surface Glycoprotein Genes in Pneumocystis ...
Pneumocystis can vary the expressed Msg, presumably as a mechanism to avoid host immune responses. Analysis of 24 msg gene sequences obtained from a single ...Missing: asci | Show results with:asci
[53]
(PDF) Biofilm Formation by Pneumocystis spp. † - ResearchGate
Aug 6, 2025 · Pneumocystis pneumonia (PCP) is a serious fungal lung infection caused by Pneumocystis jirovecii in immunosuppressed individuals. The lack ...Abstract And Figures · References (70) · Recommended Publications
[54]
De Novo Assembly of the Pneumocystis jirovecii Genome from a ...
We report here the genome of P. jirovecii that was obtained from a single bronchoalveolar lavage fluid specimen from a patient.
[55]
Sequencing and characterization of the complete mitochondrial ...
Our study shows that P. carinii and P. murina mtDNA share a nearly identical number and order of genes in a linear configuration, whereas P. jirovecii has a ...Missing: distinction | Show results with:distinction
[56]
Variation in the Major Surface Glycoprotein Genes in Pneumocystis ...
Variation in the Major Surface Glycoprotein Genes in Pneumocystis jirovecii ... Variation of the expressed Msg presumably facilitates evasion of immune ...
[57]
Genome analysis of three Pneumocystis species reveals adaptation ...
Feb 22, 2016 · Pneumocystis jirovecii is a fungus that can cause life-threatening pneumonia in immunocompromised patients. Here, the authors sequence the ...
[58]
Retracing the evolution of Pneumocystis species, with a focus on the human pathogen Pneumocystis jirovecii | Microbiology and Molecular Biology Reviews
Summary of each segment:
[59]
Targeted NGS-Based Analysis of Pneumocystis jirovecii Reveals ...
Aug 17, 2022 · Current genotyping studies focused on multilocus sequence typing performed on DNA [5,6] targeting superoxide dismutase, mtLSU, or cytochrome b.2. Materials And Methods · 2.5. Sequencing Analysis · 3. ResultsMissing: taxonomic | Show results with:taxonomic<|control11|><|separator|>
[60]
Pneumocystis Pneumonia: Adult and Adolescent OIs | NIH
Sep 9, 2025 · The taxonomy of the organism has been changed; Pneumocystis carinii now refers only to the Pneumocystis that infects rats, and P. jirovecii ...
[61]
Pneumocystis Pneumonia: Causes, Symptoms & Treatment
Aug 12, 2025 · Pneumocystis pneumonia (PCP) is a lung infection that mainly affects people with weakened immune systems. The fungus Pneumocystis jirovecii ...What Is Pneumocystis... · Symptoms And Causes · Management And Treatment
[62]
A CASE OF PNEUMOCYSTIS JIROVECII PNEUMONIA IN A NON ...
If left untreated, PJP carries a 90-100% mortality risk. Interestingly, outcomes in patients without HIV are typically worse than outcomes in HIV patients. This ...Missing: rate | Show results with:rate
[63]
Features and global impact of invasive fungal infections caused by ...
Jun 27, 2024 · Global incidence has been estimated at over 400 000 cases annually. Pneumocystis jirovecii is one of a number of important fungal pathogens, ...Results · Table 2 · Annual Incidence
[64]
Pneumocystis jirovecii Pneumonia in HIV-Negative, Non-transplant ...
Jan 20, 2024 · Now, however, PJP is increasingly found in immunocompromised individuals without HIV, with up to 60% of the over 400,000 worldwide annual cases ...
[65]
Evolving epidemiology of pneumocystis pneumonia - The Lancet
May 14, 2022 · The incidence of PCP significantly increased from 2·3 to 2·6 per 100,000 population from 2014 to 2019 (1,857 to 2,172 cases, +17·0%, p < 0·0001) ...
[66]
Pneumocystis jiroveci Pneumonia (PJP) - Medscape Reference
Aug 3, 2025 · P jiroveci is one of several organisms known to cause life-threatening opportunistic infections in patients with advanced HIV infection ...
[67]
Epidemiology, Risk Factors, and Prophylaxis Use for Pneumocystis ...
Dec 18, 2023 · The use of corticosteroids—in monotherapy or in coadministration with other immunosuppressive agents—remains the principal risk factor for PJP ...Abstract · BACKGROUND · RESULTS · DISCUSSION
[68]
Early Acquisition of Pneumocystis jirovecii Colonization and ...
Pneumocystis jirovecii colonization is frequent in preterm births and could be a risk factor to develop respiratory distress syndrome among preterm infants.Abstract · PATIENTS AND METHODS · RESULTS · DISCUSSIONMissing: elderly | Show results with:elderly
[69]
Study on the Prevalence of Pneumocystis jirovecii as a Causative ...
The present study aimed to establish the prevalence of Pneumocystis jirovecii infection in human hosts with different immune status (immunocompromised and ...
[70]
Observational Analysis of a Large Cohort of Pneumocystis jirovecii ...
The most common risk groups were hematologic malignancy (32.2%), solid tumor cancers receiving chemotherapy (22.4%), and autoimmune disease with ...Missing: global | Show results with:global
[71]
Genetic and Epidemiologic Analyses of an Outbreak of ... - PubMed
Mar 1, 2022 · Over an 11-month period, we observed a rise in cases of PCP among kidney-transplant recipients (KTR), prompting an outbreak investigation.
[72]
An overview of the laboratory diagnosis of Pneumocystis jirovecii ...
PCP can be diagnosed by direct visualization of the characteristic ascus/cyst (size range: 5–8 µm) or trophic forms (size range: 1–4 µm) through microscopy by ...
[73]
Pneumocystis jirovecii Pneumonia Diagnostic Approach: Real-Life ...
Mar 28, 2023 · Microbiological PJP diagnosis has usually been based on direct-visualization techniques with different staining methods or immunofluorescence ...3. Results · 3.2. Cycle Threshold Pcr... · 4. Discussion
[74]
Combined multiplex polymerase chain reaction-based targeted next ...
Multiplex polymerase chain reaction-based targeted next-generation sequencing (mp-tNGS) is a promising tool for identifying lower respiratory tract infections, ...
[75]
Clinical features and diagnostic value of metagenomic next - Frontiers
Mar 15, 2023 · Pneumocystis jirovecii (PJ) is an opportunistic pathogenic fungus, and PJ pneumonia (PJP) is commonly found in HIV-positive patients. With the ...
[76]
Pneumocystis carinii Pneumonia in the Adult
Jan 13, 2010 · IN 1909 Chagas,1 in Brazil, described a peculiar pneumonia in a guinea pig infected with Trypanosoma cruzi that he ascribed to that parasite.
[77]
[PDF] The Pneumocystis life cycle - SciELO
Delanoë and. Delanoë (1912) only mentioned cystic forms and no refer- ence was made to non-cystic forms of Pneumocystis for a long time. In 1942, van der Meer ...
[78]
Pneumocystis carinii versus Pneumocystis jiroveci - NIH
Chagas placed it in a new genus, Schizotrypanum (7,8). In 1912, Delanoë and Delanoë at the Pasteur Institute in Paris published the first description of the ...
[79]
Pneumocystis Pneumonia - Thoracic Key
Jan 11, 2017 · Small epidemics of plasma cell interstitial pneumonitis had been noted in children in orphanages in Europe in the 1930s and following World War ...
[80]
What Caused the Epidemic of Pneumocystis Pneumonia in ...
Jun 1, 2005 · Fatalities were due to Pneumocystis. Pneumocystis pneumonia was also reported in malnourished, orphaned infants during that period. Many ...
[81]
Infections of the lung, non-granulomatous (Chapter 3)
May 5, 2016 · In fact, some of the earliest reported cases of PCP in humans occurred in malnourished European infants in the 1930s and 1940s and in infants ...
[82]
Pneumocystis Pneumonia --- Los Angeles - CDC
In the period October 1980-May 1981, 5 young men, all active homosexuals, were treated for biopsy-confirmed Pneumocystis carinii pneumonia at 3 different ...
[83]
Pneumocystis Pneumonia—Los Angeles - JAMA Network
Oct 2, 1996 · On June 4, 1981, MMWR published a report about Pneumocystis carinii pneumonia in homosexual men in Los Angeles. This was the first published ...
[84]
Pneumocystis: from a doubtful unique entity to a group of highly ...
Pneumocystis carinii was named and described as a new biological entity (Delanoë & Delanoë, 1912). The choice of the Latin name stems from the tropism of the ...
[85]
Animal Models for Pneumocystis carinii Pneumonia - HUGHES - 1989
1988. Passive immunoprophylaxis with specific monoclonal antibody confers partial protection against Pneumocystis carinii pneumonitis in animal models. J. Clin.Missing: jirovecii | Show results with:jirovecii<|separator|>
[86]
Pneumocystis Pneumonia: Pitfalls and Hindrances to Establishing a ...
Here, we provide an overview of the animal models of Pneumocystis pneumonia that were reported in the literature over the last 60 years.
[87]
Axenic Long-Term Cultivation of Pneumocystis jirovecii - MDPI
We successfully cultivated P. jirovecii under optimized cell-free conditions in a 70-day long-term culture for the first time.
[88]
Extracellular vesicle-mediated delivery of genetic material for ...
Sep 23, 2025 · Herein, we describe a novel method for the stable transformation and CRISPR/Cas9-mediated genetic editing of Pneumocystis murina utilizing ...
[89]
A therapeutic vaccine strategy to prevent Pneumocystis pneumonia ...
Several studies have demonstrated the importance of antibodies against the Pneumocystis protein antigen KEX1 in promoting protection against PCP and ...Introduction · Materials and methods · Results · Discussion